Cytokines. Medical search

Non-antibody proteins secreted by inflammatory leukocytes and some non-leukocytic cells, that act as intercellular mediators. They differ from classical hormones in that they are produced by a number of tissue or cell types rather than by specialized glands. They generally act locally in a paracrine or autocrine rather than endocrine manner.

Serum glycoprotein produced by activated MACROPHAGES and other mammalian MONONUCLEAR LEUKOCYTES. It has necrotizing activity against tumor cell lines and increases ability to reject tumor transplants. Also known as TNF-alpha, it is only 30% homologous to TNF-beta (LYMPHOTOXIN), but they share TNF RECEPTORS.

A cytokine that stimulates the growth and differentiation of B-LYMPHOCYTES and is also a growth factor for HYBRIDOMAS and plasmacytomas. It is produced by many different cells including T-LYMPHOCYTES; MONOCYTES; and FIBROBLASTS.

A soluble factor produced by MONOCYTES; MACROPHAGES, and other cells which activates T-lymphocytes and potentiates their response to mitogens or antigens. Interleukin-1 is a general term refers to either of the two distinct proteins, INTERLEUKIN-1ALPHA and INTERLEUKIN-1BETA. The biological effects of IL-1 include the ability to replace macrophage requirements for T-cell activation.

The major interferon produced by mitogenically or antigenically stimulated LYMPHOCYTES. It is structurally different from TYPE I INTERFERON and its major activity is immunoregulation. It has been implicated in the expression of CLASS II HISTOCOMPATIBILITY ANTIGENS in cells that do not normally produce them, leading to AUTOIMMUNE DISEASES.

Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.

A pathological process characterized by injury or destruction of tissues caused by a variety of cytologic and chemical reactions. It is usually manifested by typical signs of pain, heat, redness, swelling, and loss of function.

The endogenous compounds that mediate inflammation (AUTACOIDS) and related exogenous compounds including the synthetic prostaglandins (PROSTAGLANDINS, SYNTHETIC).

A cytokine produced by a variety of cell types, including T-LYMPHOCYTES; MONOCYTES; DENDRITIC CELLS; and EPITHELIAL CELLS that exerts a variety of effects on immunoregulation and INFLAMMATION. Interleukin-10 combines with itself to form a homodimeric molecule that is the biologically active form of the protein.

A soluble factor produced by activated T-LYMPHOCYTES that induces the expression of MHC CLASS II GENES and FC RECEPTORS on B-LYMPHOCYTES and causes their proliferation and differentiation. It also acts on T-lymphocytes, MAST CELLS, and several other hematopoietic lineage cells.

An interleukin-1 subtype that is synthesized as an inactive membrane-bound pro-protein. Proteolytic processing of the precursor form by CASPASE 1 results in release of the active form of interleukin-1beta from the membrane.

Subset of helper-inducer T-lymphocytes which synthesize and secrete the interleukins IL-4, IL-5, IL-6, and IL-10. These cytokines influence B-cell development and antibody production as well as augmenting humoral responses.

Soluble factors which stimulate growth-related activities of leukocytes as well as other cell types. They enhance cell proliferation and differentiation, DNA synthesis, secretion of other biologically active molecules and responses to immune and inflammatory stimuli.

RNA sequences that serve as templates for protein synthesis. Bacterial mRNAs are generally primary transcripts in that they do not require post-transcriptional processing. Eukaryotic mRNA is synthesized in the nucleus and must be exported to the cytoplasm for translation. Most eukaryotic mRNAs have a sequence of polyadenylic acid at the 3' end, referred to as the poly(A) tail. The function of this tail is not known for certain, but it may play a role in the export of mature mRNA from the nucleus as well as in helping stabilize some mRNA molecules by retarding their degradation in the cytoplasm.

Lipid-containing polysaccharides which are endotoxins and important group-specific antigens. They are often derived from the cell wall of gram-negative bacteria and induce immunoglobulin secretion. The lipopolysaccharide molecule consists of three parts: LIPID A, core polysaccharide, and O-specific chains (O ANTIGENS). When derived from Escherichia coli, lipopolysaccharides serve as polyclonal B-cell mitogens commonly used in laboratory immunology. (From Dorland, 28th ed)

A member of the CXC chemokine family that plays a role in the regulation of the acute inflammatory response. It is secreted by variety of cell types and induces CHEMOTAXIS of NEUTROPHILS and other inflammatory cells.

Class of pro-inflammatory cytokines that have the ability to attract and activate leukocytes. They can be divided into at least three structural branches: C; (CHEMOKINES, C); CC; (CHEMOKINES, CC); and CXC; (CHEMOKINES, CXC); according to variations in a shared cysteine motif.

Subset of helper-inducer T-lymphocytes which synthesize and secrete interleukin-2, gamma-interferon, and interleukin-12. Due to their ability to kill antigen-presenting cells and their lymphokine-mediated effector activity, Th1 cells are associated with vigorous delayed-type hypersensitivity reactions.

The intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GAMMA-AMINOBUTYRIC ACID-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptor-mediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway.

The relatively long-lived phagocytic cell of mammalian tissues that are derived from blood MONOCYTES. Main types are PERITONEAL MACROPHAGES; ALVEOLAR MACROPHAGES; HISTIOCYTES; KUPFFER CELLS of the liver; and OSTEOCLASTS. They may further differentiate within chronic inflammatory lesions to EPITHELIOID CELLS or may fuse to form FOREIGN BODY GIANT CELLS or LANGHANS GIANT CELLS. (from The Dictionary of Cell Biology, Lackie and Dow, 3rd ed.)

Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control (induction or repression) of gene action at the level of transcription or translation.

Strains of mice in which certain GENES of their GENOMES have been disrupted, or "knocked-out". To produce knockouts, using RECOMBINANT DNA technology, the normal DNA sequence of the gene being studied is altered to prevent synthesis of a normal gene product. Cloned cells in which this DNA alteration is successful are then injected into mouse EMBRYOS to produce chimeric mice. The chimeric mice are then bred to yield a strain in which all the cells of the mouse contain the disrupted gene. Knockout mice are used as EXPERIMENTAL ANIMAL MODELS for diseases (DISEASE MODELS, ANIMAL) and to clarify the functions of the genes.

A heterodimeric cytokine that plays a role in innate and adaptive immune responses. Interleukin-12 is a 70 kDa protein that is composed of covalently linked 40 kDa and 35 kDa subunits. It is produced by DENDRITIC CELLS; MACROPHAGES and a variety of other immune cells and plays a role in the stimulation of INTERFERON-GAMMA production by T-LYMPHOCYTES and NATURAL KILLER CELLS.

Ubiquitous, inducible, nuclear transcriptional activator that binds to enhancer elements in many different cell types and is activated by pathogenic stimuli. The NF-kappa B complex is a heterodimer composed of two DNA-binding subunits: NF-kappa B1 and relA.

Large, phagocytic mononuclear leukocytes produced in the vertebrate BONE MARROW and released into the BLOOD; contain a large, oval or somewhat indented nucleus surrounded by voluminous cytoplasm and numerous organelles.

An immunoassay utilizing an antibody labeled with an enzyme marker such as horseradish peroxidase. While either the enzyme or the antibody is bound to an immunosorbent substrate, they both retain their biologic activity; the change in enzyme activity as a result of the enzyme-antibody-antigen reaction is proportional to the concentration of the antigen and can be measured spectrophotometrically or with the naked eye. Many variations of the method have been developed.

A cytokine synthesized by T-LYMPHOCYTES that produces proliferation, immunoglobulin isotype switching, and immunoglobulin production by immature B-LYMPHOCYTES. It appears to play a role in regulating inflammatory and immune responses.

Lymphocytes responsible for cell-mediated immunity. Two types have been identified - cytotoxic (T-LYMPHOCYTES, CYTOTOXIC) and helper T-lymphocytes (T-LYMPHOCYTES, HELPER-INDUCER). They are formed when lymphocytes circulate through the THYMUS GLAND and differentiate to thymocytes. When exposed to an antigen, they divide rapidly and produce large numbers of new T cells sensitized to that antigen.

Naturally occurring or experimentally induced animal diseases with pathological processes sufficiently similar to those of human diseases. They are used as study models for human diseases.

A soluble substance elaborated by antigen- or mitogen-stimulated T-LYMPHOCYTES which induces DNA synthesis in naive lymphocytes.

Morphologic alteration of small B LYMPHOCYTES or T LYMPHOCYTES in culture into large blast-like cells able to synthesize DNA and RNA and to divide mitotically. It is induced by INTERLEUKINS; MITOGENS such as PHYTOHEMAGGLUTININS, and by specific ANTIGENS. It may also occur in vivo as in GRAFT REJECTION.

An acidic glycoprotein of MW 23 kDa with internal disulfide bonds. The protein is produced in response to a number of inflammatory mediators by mesenchymal cells present in the hemopoietic environment and at peripheral sites of inflammation. GM-CSF is able to stimulate the production of neutrophilic granulocytes, macrophages, and mixed granulocyte-macrophage colonies from bone marrow cells and can stimulate the formation of eosinophil colonies from fetal liver progenitor cells. GM-CSF can also stimulate some functional activities in mature granulocytes and macrophages.

A proinflammatory cytokine produced primarily by T-LYMPHOCYTES or their precursors. Several subtypes of interleukin-17 have been identified, each of which is a product of a unique gene.

Technique using an instrument system for making, processing, and displaying one or more measurements on individual cells obtained from a cell suspension. Cells are usually stained with one or more fluorescent dyes specific to cell components of interest, e.g., DNA, and fluorescence of each cell is measured as it rapidly transverses the excitation beam (laser or mercury arc lamp). Fluorescence provides a quantitative measure of various biochemical and biophysical properties of the cell, as well as a basis for cell sorting. Other measurable optical parameters include light absorption and light scattering, the latter being applicable to the measurement of cell size, shape, density, granularity, and stain uptake.

Specialized cells of the hematopoietic system that have branch-like extensions. They are found throughout the lymphatic system, and in non-lymphoid tissues such as SKIN and the epithelia of the intestinal, respiratory, and reproductive tracts. They trap and process ANTIGENS, and present them to T-CELLS, thereby stimulating CELL-MEDIATED IMMUNITY. They are different from the non-hematopoietic FOLLICULAR DENDRITIC CELLS, which have a similar morphology and immune system function, but with respect to humoral immunity (ANTIBODY PRODUCTION).

A variation of the PCR technique in which cDNA is made from RNA via reverse transcription. The resultant cDNA is then amplified using standard PCR protocols.

Established cell cultures that have the potential to propagate indefinitely.

A positive regulatory effect on physiological processes at the molecular, cellular, or systemic level. At the molecular level, the major regulatory sites include membrane receptors, genes (GENE EXPRESSION REGULATION), mRNAs (RNA, MESSENGER), and proteins.

Mature LYMPHOCYTES and MONOCYTES transported by the blood to the body's extravascular space. They are morphologically distinguishable from mature granulocytic leukocytes by their large, non-lobed nuclei and lack of coarse, heavily stained cytoplasmic granules.

The capacity of a normal organism to remain unaffected by microorganisms and their toxins. It results from the presence of naturally occurring ANTI-INFECTIVE AGENTS, constitutional factors such as BODY TEMPERATURE and immediate acting immune cells such as NATURAL KILLER CELLS.

Cell surface proteins that bind cytokines and trigger intracellular changes influencing the behavior of cells.

The phenotypic manifestation of a gene or genes by the processes of GENETIC TRANSCRIPTION and GENETIC TRANSLATION.

A critical subpopulation of T-lymphocytes involved in the induction of most immunological functions. The HIV virus has selective tropism for the T4 cell which expresses the CD4 phenotypic marker, a receptor for HIV. In fact, the key element in the profound immunosuppression seen in HIV infection is the depletion of this subset of T-lymphocytes.

A cytokine that promotes differentiation and activation of EOSINOPHILS. It also triggers activated B-LYMPHOCYTES to differentiate into IMMUNOGLOBULIN-secreting cells.

Progressive restriction of the developmental potential and increasing specialization of function that leads to the formation of specialized cells, tissues, and organs.

Proteins prepared by recombinant DNA technology.

Differentiation antigens residing on mammalian leukocytes. CD stands for cluster of differentiation, which refers to groups of monoclonal antibodies that show similar reactivity with certain subpopulations of antigens of a particular lineage or differentiation stage. The subpopulations of antigens are also known by the same CD designation.

A factor synthesized in a wide variety of tissues. It acts synergistically with TGF-alpha in inducing phenotypic transformation and can also act as a negative autocrine growth factor. TGF-beta has a potential role in embryonal development, cellular differentiation, hormone secretion, and immune function. TGF-beta is found mostly as homodimer forms of separate gene products TGF-beta1, TGF-beta2 or TGF-beta3. Heterodimers composed of TGF-beta1 and 2 (TGF-beta1.2) or of TGF-beta2 and 3 (TGF-beta2.3) have been isolated. The TGF-beta proteins are synthesized as precursor proteins.

A cytokine which resembles IL-1 structurally and IL-12 functionally. It enhances the cytotoxic activity of NK CELLS and CYTOTOXIC T-LYMPHOCYTES, and appears to play a role both as neuroimmunomodulator and in the induction of mucosal immunity.

Either of the pair of organs occupying the cavity of the thorax that effect the aeration of the blood.

A chemokine that is a chemoattractant for MONOCYTES and may also cause cellular activation of specific functions related to host defense. It is produced by LEUKOCYTES of both monocyte and lymphocyte lineage and by FIBROBLASTS during tissue injury. It has specificity for CCR2 RECEPTORS.

An encapsulated lymphatic organ through which venous blood filters.

A family of pattern recognition receptors characterized by an extracellular leucine-rich domain and a cytoplasmic domain that share homology with the INTERLEUKIN 1 RECEPTOR and the DROSOPHILA toll protein. Following pathogen recognition, toll-like receptors recruit and activate a variety of SIGNAL TRANSDUCING ADAPTOR PROTEINS.

A ligand that binds to but fails to activate the INTERLEUKIN 1 RECEPTOR. It plays an inhibitory role in the regulation of INFLAMMATION and FEVER. Several isoforms of the protein exist due to multiple ALTERNATIVE SPLICING of its mRNA.

Substances that reduce or suppress INFLAMMATION.

Subset of helper-effector T-lymphocytes which synthesize and secrete IL-17, IL-17F, and IL-22. These cytokines are involved in host defenses and tissue inflammation in autoimmune diseases.

A cytokine receptor that acts through the formation of oligomeric complexes of itself with a variety of CYTOKINE RECEPTORS.

Glycoproteins found on the membrane or surface of cells.

The process of altering the morphology and functional activity of macrophages so that they become avidly phagocytic. It is initiated by lymphokines, such as the macrophage activation factor (MAF) and the macrophage migration-inhibitory factor (MMIF), immune complexes, C3b, and various peptides, polysaccharides, and immunologic adjuvants.

Elements of limited time intervals, contributing to particular results or situations.

A pattern recognition receptor that interacts with LYMPHOCYTE ANTIGEN 96 and LIPOPOLYSACCHARIDES. It mediates cellular responses to GRAM-NEGATIVE BACTERIA.

A technique of culturing mixed cell types in vitro to allow their synergistic or antagonistic interactions, such as on CELL DIFFERENTIATION or APOPTOSIS. Coculture can be of different types of cells, tissues, or organs from normal or disease states.

One of the mechanisms by which CELL DEATH occurs (compare with NECROSIS and AUTOPHAGOCYTOSIS). Apoptosis is the mechanism responsible for the physiological deletion of cells and appears to be intrinsically programmed. It is characterized by distinctive morphologic changes in the nucleus and cytoplasm, chromatin cleavage at regularly spaced sites, and the endonucleolytic cleavage of genomic DNA; (DNA FRAGMENTATION); at internucleosomal sites. This mode of cell death serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth.

An interleukin-1 subtype that occurs as a membrane-bound pro-protein form that is cleaved by proteases to form a secreted mature form. Unlike INTERLEUKIN-1BETA both membrane-bound and secreted forms of interleukin-1alpha are biologically active.

Cell surface proteins that bind interleukins and trigger intracellular changes influencing the behavior of cells.

Measurable and quantifiable biological parameters (e.g., specific enzyme concentration, specific hormone concentration, specific gene phenotype distribution in a population, presence of biological substances) which serve as indices for health- and physiology-related assessments, such as disease risk, psychiatric disorders, environmental exposure and its effects, disease diagnosis, metabolic processes, substance abuse, pregnancy, cell line development, epidemiologic studies, etc.

Laboratory mice that have been produced from a genetically manipulated EGG or EMBRYO, MAMMALIAN.

Granular leukocytes having a nucleus with three to five lobes connected by slender threads of chromatin, and cytoplasm containing fine inconspicuous granules and stainable by neutral dyes.

A cytokine with both pro- and anti-inflammatory actions that depend upon the cellular microenvironment. Oncostatin M is a 28 kDa monomeric glycoprotein that is similar in structure to LEUKEMIA INHIBITORY FACTOR. Its name derives from the the observation that it inhibited the growth of tumor cells and augmented the growth of normal fibroblasts.

Biologically active substances whose activities affect or play a role in the functioning of the immune system.

A lymphohematopoietic cytokine that plays a role in regulating the proliferation of ERYTHROID PRECURSOR CELLS. It induces maturation of MEGAKARYOCYTES which results in increased production of BLOOD PLATELETS. Interleukin-11 was also initially described as an inhibitor of ADIPOGENESIS of cultured preadipocytes.

A negative regulatory effect on physiological processes at the molecular, cellular, or systemic level. At the molecular level, the major regulatory sites include membrane receptors, genes (GENE EXPRESSION REGULATION), mRNAs (RNA, MESSENGER), and proteins.

A CALCIUM-independent subtype of nitric oxide synthase that may play a role in immune function. It is an inducible enzyme whose expression is transcriptionally regulated by a variety of CYTOKINES.

Substances that augment, stimulate, activate, potentiate, or modulate the immune response at either the cellular or humoral level. The classical agents (Freund's adjuvant, BCG, Corynebacterium parvum, et al.) contain bacterial antigens. Some are endogenous (e.g., histamine, interferon, transfer factor, tuftsin, interleukin-1). Their mode of action is either non-specific, resulting in increased immune responsiveness to a wide variety of antigens, or antigen-specific, i.e., affecting a restricted type of immune response to a narrow group of antigens. The therapeutic efficacy of many biological response modifiers is related to their antigen-specific immunoadjuvanticity.

A classification of T-lymphocytes, especially into helper/inducer, suppressor/effector, and cytotoxic subsets, based on structurally or functionally different populations of cells.

Mononuclear phagocytes derived from bone marrow precursors but resident in the peritoneum.

Cell surface receptors that are specific for INTERLEUKIN-1. Included under this heading are signaling receptors, non-signaling receptors and accessory proteins required for receptor signaling. Signaling from interleukin-1 receptors occurs via interaction with SIGNAL TRANSDUCING ADAPTOR PROTEINS such as MYELOID DIFFERENTIATION FACTOR 88.

Homeostatic control of the immune system by secretion of different cytokines by the Th1 and Th2 cells. The concentration dependent binding of the various cytokines to specific receptors determines the balance (or imbalance leading to disease).

Cytokine that stimulates the proliferation of T-LYMPHOCYTES and shares biological activities with IL-2. IL-15 also can induce proliferation and differentiation of B-LYMPHOCYTES.

A signal transducer and activator of transcription that mediates cellular responses to INTERLEUKIN-6 family members. STAT3 is constitutively activated in a variety of TUMORS and is a major downstream transducer for the CYTOKINE RECEPTOR GP130.

A critical subpopulation of regulatory T-lymphocytes involved in MHC Class I-restricted interactions. They include both cytotoxic T-lymphocytes (T-LYMPHOCYTES, CYTOTOXIC) and CD8+ suppressor T-lymphocytes.

The fission of a CELL. It includes CYTOKINESIS, when the CYTOPLASM of a cell is divided, and CELL NUCLEUS DIVISION.

Cells that line the inner and outer surfaces of the body by forming cellular layers (EPITHELIUM) or masses. Epithelial cells lining the SKIN; the MOUTH; the NOSE; and the ANAL CANAL derive from ectoderm; those lining the RESPIRATORY SYSTEM and the DIGESTIVE SYSTEM derive from endoderm; others (CARDIOVASCULAR SYSTEM and LYMPHATIC SYSTEM) derive from mesoderm. Epithelial cells can be classified mainly by cell shape and function into squamous, glandular and transitional epithelial cells.

Subpopulation of CD4+ lymphocytes that cooperate with other lymphocytes (either T or B) to initiate a variety of immune functions. For example, helper-inducer T-cells cooperate with B-cells to produce antibodies to thymus-dependent antigens and with other subpopulations of T-cells to initiate a variety of cell-mediated immune functions.

A multilineage cell growth factor secreted by LYMPHOCYTES; EPITHELIAL CELLS; and ASTROCYTES which stimulates clonal proliferation and differentiation of various types of blood and tissue cells.

An INTERLEUKIN-6 related cytokine that exhibits pleiotrophic effects on many physiological systems that involve cell proliferation, differentiation, and survival. Leukemia inhibitory factor binds to and acts through the lif receptor.

Cell surface receptors that are specific for INTERLEUKIN-6. They are present on T-LYMPHOCYTES, mitogen-activated B-LYMPHOCYTES, and peripheral MONOCYTES. The receptors are heterodimers of the INTERLEUKIN-6 RECEPTOR ALPHA SUBUNIT and the CYTOKINE RECEPTOR GP130.

All of the processes involved in increasing CELL NUMBER including CELL DIVISION.

A free radical gas produced endogenously by a variety of mammalian cells, synthesized from ARGININE by NITRIC OXIDE SYNTHASE. Nitric oxide is one of the ENDOTHELIUM-DEPENDENT RELAXING FACTORS released by the vascular endothelium and mediates VASODILATION. It also inhibits platelet aggregation, induces disaggregation of aggregated platelets, and inhibits platelet adhesion to the vascular endothelium. Nitric oxide activates cytosolic GUANYLATE CYCLASE and thus elevates intracellular levels of CYCLIC GMP.

Bone marrow-derived lymphocytes that possess cytotoxic properties, classically directed against transformed and virus-infected cells. Unlike T CELLS; and B CELLS; NK CELLS are not antigen specific. The cytotoxicity of natural killer cells is determined by the collective signaling of an array of inhibitory and stimulatory CELL SURFACE RECEPTORS. A subset of T-LYMPHOCYTES referred to as NATURAL KILLER T CELLS shares some of the properties of this cell type.

A pattern recognition receptor that forms heterodimers with other TOLL-LIKE RECEPTORS. It interacts with multiple ligands including PEPTIDOGLYCAN, bacterial LIPOPROTEINS, lipoarabinomannan, and a variety of PORINS.

Washing liquid obtained from irrigation of the lung, including the BRONCHI and the PULMONARY ALVEOLI. It is generally used to assess biochemical, inflammatory, or infection status of the lung.

Histochemical localization of immunoreactive substances using labeled antibodies as reagents.

Cells contained in the bone marrow including fat cells (see ADIPOCYTES); STROMAL CELLS; MEGAKARYOCYTES; and the immediate precursors of most blood cells.

A chronic systemic disease, primarily of the joints, marked by inflammatory changes in the synovial membranes and articular structures, widespread fibrinoid degeneration of the collagen fibers in mesenchymal tissues, and by atrophy and rarefaction of bony structures. Etiology is unknown, but autoimmune mechanisms have been implicated.

Culture media containing biologically active components obtained from previously cultured cells or tissues that have released into the media substances affecting certain cell functions (e.g., growth, lysis).

Connective tissue cells which secrete an extracellular matrix rich in collagen and other macromolecules.

Identification of proteins or peptides that have been electrophoretically separated by blot transferring from the electrophoresis gel to strips of nitrocellulose paper, followed by labeling with antibody probes.

The relationship between the dose of an administered drug and the response of the organism to the drug.

The inner membrane of a joint capsule surrounding a freely movable joint. It is loosely attached to the external fibrous capsule and secretes SYNOVIAL FLUID.

The body's defense mechanism against foreign organisms or substances and deviant native cells. It includes the humoral immune response and the cell-mediated response and consists of a complex of interrelated cellular, molecular, and genetic components.

The third type of glial cell, along with astrocytes and oligodendrocytes (which together form the macroglia). Microglia vary in appearance depending on developmental stage, functional state, and anatomical location; subtype terms include ramified, perivascular, ameboid, resting, and activated. Microglia clearly are capable of phagocytosis and play an important role in a wide spectrum of neuropathologies. They have also been suggested to act in several other roles including in secretion (e.g., of cytokines and neural growth factors), in immunological processing (e.g., antigen presentation), and in central nervous system development and remodeling.

A heterodimeric cytokine that plays a role in innate and adaptive immune responses. Interleukin-23 is comprised of a unique 19 kDa subunit and 40 kDa subunit that is shared with INTERLEUKIN-12. It is produced by DENDRITIC CELLS; MACROPHAGES and a variety of other immune cells

The span of viability of a cell characterized by the capacity to perform certain functions such as metabolism, growth, reproduction, some form of responsiveness, and adaptability.

Process of classifying cells of the immune system based on structural and functional differences. The process is commonly used to analyze and sort T-lymphocytes into subsets based on CD antigens by the technique of flow cytometry.

Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.

White blood cells. These include granular leukocytes (BASOPHILS; EOSINOPHILS; and NEUTROPHILS) as well as non-granular leukocytes (LYMPHOCYTES and MONOCYTES).

Endogenous or exogenous substances which inhibit the normal growth of human and animal cells or micro-organisms, as distinguished from those affecting plant growth (= PLANT GROWTH REGULATORS).

A cell-surface ligand involved in leukocyte adhesion and inflammation. Its production is induced by gamma-interferon and it is required for neutrophil migration into inflamed tissue.

The outer covering of the body that protects it from the environment. It is composed of the DERMIS and the EPIDERMIS.

Cells grown in vitro from neoplastic tissue. If they can be established as a TUMOR CELL LINE, they can be propagated in cell culture indefinitely.

Granular leukocytes with a nucleus that usually has two lobes connected by a slender thread of chromatin, and cytoplasm containing coarse, round granules that are uniform in size and stainable by eosin.

Cell surface receptors that bind TUMOR NECROSIS FACTORS and trigger changes which influence the behavior of cells.

A cytokine produced by bone marrow stromal cells that promotes the growth of B-LYMPHOCYTE precursors and is co-mitogenic with INTERLEUKIN-2 for mature T-LYMPHOCYTE activation.

A mitogen-activated protein kinase subfamily that regulates a variety of cellular processes including CELL GROWTH PROCESSES; CELL DIFFERENTIATION; APOPTOSIS; and cellular responses to INFLAMMATION. The P38 MAP kinases are regulated by CYTOKINE RECEPTORS and can be activated in response to bacterial pathogens.

A signal transducer and activator of transcription that mediates cellular responses to INTERLEUKIN-4. Stat6 has been shown to partner with NF-KAPPA B and CCAAT-ENHANCER-BINDING PROTEINS to regulate GENETIC TRANSCRIPTION of interleukin-4 responsive GENES.

A family of structurally related proteins that are induced by CYTOKINES and negatively regulate cytokine-mediated SIGNAL TRANSDUCTION PATHWAYS. SOCS proteins contain a central SH2 DOMAIN and a C-terminal region of homology known as the SOCS box.

The biochemical and electrophysiological interactions between the NERVOUS SYSTEM and IMMUNE SYSTEM.

A strain of albino rat used widely for experimental purposes because of its calmness and ease of handling. It was developed by the Sprague-Dawley Animal Company.

An albumin obtained from the white of eggs. It is a member of the serpin superfamily.

Signal molecules that are involved in the control of cell growth and differentiation.

Glycolipid-anchored membrane glycoproteins expressed on cells of the myelomonocyte lineage including monocytes, macrophages, and some granulocytes. They function as receptors for the complex of lipopolysaccharide (LPS) and LPS-binding protein.

Toxins closely associated with the living cytoplasm or cell wall of certain microorganisms, which do not readily diffuse into the culture medium, but are released upon lysis of the cells.

A signal transducer and activator of transcription that mediates cellular responses to INTERFERONS. Stat1 interacts with P53 TUMOR SUPPRESSOR PROTEIN and regulates expression of GENES involved in growth control and APOPTOSIS.

Antibodies produced by a single clone of cells.

A CC-type chemokine that is a chemoattractant for EOSINOPHILS; MONOCYTES; and LYMPHOCYTES. It is a potent and selective eosinophil chemotaxin that is stored in and released from PLATELETS and activated T-LYMPHOCYTES. Chemokine CCL5 is specific for CCR1 RECEPTORS; CCR3 RECEPTORS; and CCR5 RECEPTORS. The acronym RANTES refers to Regulated on Activation, Normal T Expressed and Secreted.

A hematopoietic growth factor and the ligand of the cell surface c-kit protein (PROTO-ONCOGENE PROTEINS C-KIT). It is expressed during embryogenesis and is a growth factor for a number of cell types including the MAST CELLS and the MELANOCYTES in addition to the HEMATOPOIETIC STEM CELLS.

Glycoproteins which contain sialic acid as one of their carbohydrates. They are often found on or in the cell or tissue membranes and participate in a variety of biological activities.

The biosynthesis of RNA carried out on a template of DNA. The biosynthesis of DNA from an RNA template is called REVERSE TRANSCRIPTION.

A CC chemokine with specificity for CCR5 RECEPTORS. It is a chemoattractant for NK CELLS; MONOCYTES and a variety of other immune cells. This chemokine is encoded by multiple genes.

A tumor necrosis factor family member that is released by activated LYMPHOCYTES. Soluble lymphotoxin is specific for TUMOR NECROSIS FACTOR RECEPTOR TYPE I; TUMOR NECROSIS FACTOR RECEPTOR TYPE II; and TUMOR NECROSIS FACTOR RECEPTOR SUPERFAMILY, MEMBER 14. Lymphotoxin-alpha can form a membrane-bound heterodimer with LYMPHOTOXIN-BETA that has specificity for the LYMPHOTOXIN BETA RECEPTOR.

The action of a drug in promoting or enhancing the effectiveness of another drug.

An immunoglobulin associated with MAST CELLS. Overexpression has been associated with allergic hypersensitivity (HYPERSENSITIVITY, IMMEDIATE).

Lymphoid cells concerned with humoral immunity. They are short-lived cells resembling bursa-derived lymphocytes of birds in their production of immunoglobulin upon appropriate stimulation.

The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.

A large lobed glandular organ in the abdomen of vertebrates that is responsible for detoxification, metabolism, synthesis and storage of various substances.

The movement of cells from one location to another. Distinguish from CYTOKINESIS which is the process of dividing the CYTOPLASM of a cell.

Progenitor cells from which all blood cells derive.

An intracellular signaling adaptor protein that plays a role in TOLL-LIKE RECEPTOR and INTERLEUKIN 1 RECEPTORS signal transduction. It forms a signaling complex with the activated cell surface receptors and members of the IRAK KINASES.

Proteins which bind to DNA. The family includes proteins which bind to both double- and single-stranded DNA and also includes specific DNA binding proteins in serum which can be used as markers for malignant diseases.

Soluble mediators of the immune response that are neither antibodies nor complement. They are produced largely, but not exclusively, by monocytes and macrophages.

One of the type I interferons produced by peripheral blood leukocytes or lymphoblastoid cells. In addition to antiviral activity, it activates NATURAL KILLER CELLS and B-LYMPHOCYTES, and down-regulates VASCULAR ENDOTHELIAL GROWTH FACTOR expression through PI-3 KINASE and MAPK KINASES signaling pathways.

Diffusible gene products that act on homologous or heterologous molecules of viral or cellular DNA to regulate the expression of proteins.

Disorders that are characterized by the production of antibodies that react with host tissues or immune effector cells that are autoreactive to endogenous peptides.

Heparin-binding proteins that exhibit a number of inflammatory and immunoregulatory activities. Originally identified as secretory products of MACROPHAGES, these chemokines are produced by a variety of cell types including NEUTROPHILS; FIBROBLASTS; and EPITHELIAL CELLS. They likely play a significant role in respiratory tract defenses.

Methods for maintaining or growing CELLS in vitro.

Manifestations of the immune response which are mediated by antigen-sensitized T-lymphocytes via lymphokines or direct cytotoxicity. This takes place in the absence of circulating antibody or where antibody plays a subordinate role.

The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety.

Surface ligands, usually glycoproteins, that mediate cell-to-cell adhesion. Their functions include the assembly and interconnection of various vertebrate systems, as well as maintenance of tissue integration, wound healing, morphogenic movements, cellular migrations, and metastasis.

A common genetically determined, chronic, inflammatory skin disease characterized by rounded erythematous, dry, scaling patches. The lesions have a predilection for nails, scalp, genitalia, extensor surfaces, and the lumbosacral region. Accelerated epidermopoiesis is considered to be the fundamental pathologic feature in psoriasis.

An NADPH-dependent enzyme that catalyzes the conversion of L-ARGININE and OXYGEN to produce CITRULLINE and NITRIC OXIDE.

An early local inflammatory reaction to insult or injury that consists of fever, an increase in inflammatory humoral factors, and an increased synthesis by hepatocytes of a number of proteins or glycoproteins usually found in the plasma.

Systemic inflammatory response syndrome with a proven or suspected infectious etiology. When sepsis is associated with organ dysfunction distant from the site of infection, it is called severe sepsis. When sepsis is accompanied by HYPOTENSION despite adequate fluid infusion, it is called SEPTIC SHOCK.

CD4-positive T cells that inhibit immunopathology or autoimmune disease in vivo. They inhibit the immune response by influencing the activity of other cell types. Regulatory T-cells include naturally occurring CD4+CD25+ cells, IL-10 secreting Tr1 cells, and Th3 cells.

Methods used for detecting the amplified DNA products from the polymerase chain reaction as they accumulate instead of at the end of the reaction.

Granulated cells that are found in almost all tissues, most abundantly in the skin and the gastrointestinal tract. Like the BASOPHILS, mast cells contain large amounts of HISTAMINE and HEPARIN. Unlike basophils, mast cells normally remain in the tissues and do not circulate in the blood. Mast cells, derived from the bone marrow stem cells, are regulated by the STEM CELL FACTOR.

Cell surface proteins that bind signalling molecules external to the cell with high affinity and convert this extracellular event into one or more intracellular signals that alter the behavior of the target cell (From Alberts, Molecular Biology of the Cell, 2nd ed, pp693-5). Cell surface receptors, unlike enzymes, do not chemically alter their ligands.

In vitro method for producing large amounts of specific DNA or RNA fragments of defined length and sequence from small amounts of short oligonucleotide flanking sequences (primers). The essential steps include thermal denaturation of the double-stranded target molecules, annealing of the primers to their complementary sequences, and extension of the annealed primers by enzymatic synthesis with DNA polymerase. The reaction is efficient, specific, and extremely sensitive. Uses for the reaction include disease diagnosis, detection of difficult-to-isolate pathogens, mutation analysis, genetic testing, DNA sequencing, and analyzing evolutionary relationships.

Single pavement layer of cells which line the luminal surface of the entire vascular system and regulate the transport of macromolecules and blood components.

Round, granular, mononuclear phagocytes found in the alveoli of the lungs. They ingest small inhaled particles resulting in degradation and presentation of the antigen to immunocompetent cells.

Lining of the INTESTINES, consisting of an inner EPITHELIUM, a middle LAMINA PROPRIA, and an outer MUSCULARIS MUCOSAE. In the SMALL INTESTINE, the mucosa is characterized by a series of folds and abundance of absorptive cells (ENTEROCYTES) with MICROVILLI.

Soluble protein factors generated by activated lymphocytes that affect other cells, primarily those involved in cellular immunity.

Group of chemokines with paired cysteines separated by a different amino acid. CXC chemokines are chemoattractants for neutrophils but not monocytes.

The most common and most biologically active of the mammalian prostaglandins. It exhibits most biological activities characteristic of prostaglandins and has been used extensively as an oxytocic agent. The compound also displays a protective effect on the intestinal mucosa.

Any of several ways in which living cells of an organism communicate with one another, whether by direct contact between cells or by means of chemical signals carried by neurotransmitter substances, hormones, and cyclic AMP.

A cytokine subunit that is a component of both interleukin-12 and interleukin-23. It binds to the INTERLEUKIN-12 SUBUNIT P35 via a disulfide bond to form interleukin-12 and to INTERLEUKIN-23 SUBUNIT P19 to form interleukin-23.

Anti-inflammatory agents that are non-steroidal in nature. In addition to anti-inflammatory actions, they have analgesic, antipyretic, and platelet-inhibitory actions.They act by blocking the synthesis of prostaglandins by inhibiting cyclooxygenase, which converts arachidonic acid to cyclic endoperoxides, precursors of prostaglandins. Inhibition of prostaglandin synthesis accounts for their analgesic, antipyretic, and platelet-inhibitory actions; other mechanisms may contribute to their anti-inflammatory effects.

A specific immune response elicited by a specific dose of an immunologically active substance or cell in an organism, tissue, or cell.

White blood cells formed in the body's lymphoid tissue. The nucleus is round or ovoid with coarse, irregularly clumped chromatin while the cytoplasm is typically pale blue with azurophilic (if any) granules. Most lymphocytes can be classified as either T or B (with subpopulations of each), or NATURAL KILLER CELLS.

The determination of the pattern of genes expressed at the level of GENETIC TRANSCRIPTION, under specific circumstances or in a specific cell.

A cell line derived from cultured tumor cells.

The specific failure of a normally responsive individual to make an immune response to a known antigen. It results from previous contact with the antigen by an immunologically immature individual (fetus or neonate) or by an adult exposed to extreme high-dose or low-dose antigen, or by exposure to radiation, antimetabolites, antilymphocytic serum, etc.

Cell surface receptors for INTERLEUKIN-17. Several subtypes of receptors have been found, each with its own in specificity for interleukin-17 subtype.

A subtype of transforming growth factor beta that is synthesized by a wide variety of cells. It is synthesized as a precursor molecule that is cleaved to form mature TGF-beta 1 and TGF-beta1 latency-associated peptide. The association of the cleavage products results in the formation a latent protein which must be activated to bind its receptor. Defects in the gene that encodes TGF-beta1 are the cause of CAMURATI-ENGELMANN SYNDROME.

Altered reactivity to an antigen, which can result in pathologic reactions upon subsequent exposure to that particular antigen.

Proteins which are found in membranes including cellular and intracellular membranes. They consist of two types, peripheral and integral proteins. They include most membrane-associated enzymes, antigenic proteins, transport proteins, and drug, hormone, and lectin receptors.

A CXC chemokine that is induced by GAMMA-INTERFERON and is chemotactic for MONOCYTES and T-LYMPHOCYTES. It has specificity for the CXCR3 RECEPTOR.

A CXC chemokine with specificity for CXCR2 RECEPTORS. It has growth factor activities and is implicated as a oncogenic factor in several tumor types.

Regulatory proteins and peptides that are signaling molecules involved in the process of PARACRINE COMMUNICATION. They are generally considered factors that are expressed by one cell and are responded to by receptors on another nearby cell. They are distinguished from HORMONES in that their actions are local rather than distal.

Short sequences (generally about 10 base pairs) of DNA that are complementary to sequences of messenger RNA and allow reverse transcriptases to start copying the adjacent sequences of mRNA. Primers are used extensively in genetic and molecular biology techniques.

A CC chemokine with specificity for CCR1 RECEPTORS and CCR5 RECEPTORS. It is a chemoattractant for NK CELLS; MONOCYTES; and a variety of other immune cells. This chemokine is encoded by multiple genes.

Complex of at least five membrane-bound polypeptides in mature T-lymphocytes that are non-covalently associated with one another and with the T-cell receptor (RECEPTORS, ANTIGEN, T-CELL). The CD3 complex includes the gamma, delta, epsilon, zeta, and eta chains (subunits). When antigen binds to the T-cell receptor, the CD3 complex transduces the activating signals to the cytoplasm of the T-cell. The CD3 gamma and delta chains (subunits) are separate from and not related to the gamma/delta chains of the T-cell receptor (RECEPTORS, ANTIGEN, T-CELL, GAMMA-DELTA).

ARTHRITIS that is induced in experimental animals. Immunological methods and infectious agents can be used to develop experimental arthritis models. These methods include injections of stimulators of the immune response, such as an adjuvant (ADJUVANTS, IMMUNOLOGIC) or COLLAGEN.

The major immunoglobulin isotype class in normal human serum. There are several isotype subclasses of IgG, for example, IgG1, IgG2A, and IgG2B.

A mononuclear phagocyte colony-stimulating factor (M-CSF) synthesized by mesenchymal cells. The compound stimulates the survival, proliferation, and differentiation of hematopoietic cells of the monocyte-macrophage series. M-CSF is a disulfide-bonded glycoprotein dimer with a MW of 70 kDa. It binds to a specific high affinity receptor (RECEPTOR, MACROPHAGE COLONY-STIMULATING FACTOR).

A superfamily of PROTEIN-SERINE-THREONINE KINASES that are activated by diverse stimuli via protein kinase cascades. They are the final components of the cascades, activated by phosphorylation by MITOGEN-ACTIVATED PROTEIN KINASE KINASES, which in turn are activated by mitogen-activated protein kinase kinase kinases (MAP KINASE KINASE KINASES).

Chemical substances that attract or repel cells. The concept denotes especially those factors released as a result of tissue injury, microbial invasion, or immunologic activity, that attract LEUKOCYTES; MACROPHAGES; or other cells to the site of infection or insult.

Inflammation of the COLON section of the large intestine (INTESTINE, LARGE), usually with symptoms such as DIARRHEA (often with blood and mucus), ABDOMINAL PAIN, and FEVER.

Immunoglobulin molecules having a specific amino acid sequence by virtue of which they interact only with the ANTIGEN (or a very similar shape) that induced their synthesis in cells of the lymphoid series (especially PLASMA CELLS).

Interferon secreted by leukocytes, fibroblasts, or lymphoblasts in response to viruses or interferon inducers other than mitogens, antigens, or allo-antigens. They include alpha- and beta-interferons (INTERFERON-ALPHA and INTERFERON-BETA).

Conversion of an inactive form of an enzyme to one possessing metabolic activity. It includes 1, activation by ions (activators); 2, activation by cofactors (coenzymes); and 3, conversion of an enzyme precursor (proenzyme or zymogen) to an active enzyme.

Endogenously-synthesized compounds that influence biological processes not otherwise classified under ENZYMES; HORMONES or HORMONE ANTAGONISTS.

Process whereby the immune system reacts against the body's own tissues. Autoimmunity may produce or be caused by AUTOIMMUNE DISEASES.

A family of inhibitory proteins which bind to the REL PROTO-ONCOGENE PROTEINS and modulate their activity. In the CYTOPLASM, I-kappa B proteins bind to the transcription factor NF-KAPPA B. Cell stimulation causes its dissociation and translocation of active NF-kappa B to the nucleus.

Sepsis associated with HYPOTENSION or hypoperfusion despite adequate fluid resuscitation. Perfusion abnormalities may include, but are not limited to LACTIC ACIDOSIS; OLIGURIA; or acute alteration in mental status.

An anti-inflammatory 9-fluoro-glucocorticoid.

GM-CSF-deficient mice are susceptible to pulmonary group B streptococcal infection. (1/33104)

Granulocyte-macrophage colony-stimulating factor (GM-CSF) gene-targeted mice (GM-/-) cleared group B streptococcus (GBS) from the lungs more slowly than wild-type mice. Expression of GM-CSF in the respiratory epithelium of GM-/- mice improved bacterial clearance to levels greater than that in wild-type GM+/+ mice. Acute aerosolization of GM-CSF to GM+/+ mice significantly enhanced clearance of GBS at 24 hours. GBS infection was associated with increased neutrophilic infiltration in lungs of GM-/- mice, while macrophage infiltrates predominated in wild-type mice, suggesting an abnormality in macrophage clearance of bacteria in the absence of GM-CSF. While phagocytosis of GBS was unaltered, production of superoxide radicals and hydrogen peroxide was markedly deficient in macrophages from GM-/- mice. Lipid peroxidation, assessed by measuring the isoprostane 8-iso-PGF2alpha, was decreased in the lungs of GM-/- mice. GM-CSF plays an important role in GBS clearance in vivo, mediated in part by its role in enhancing superoxide and hydrogen peroxide production and bacterial killing by alveolar macrophages. (+info)

Socs1 binds to multiple signalling proteins and suppresses steel factor-dependent proliferation. (2/33104)

We have identified Socs1 as a downstream component of the Kit receptor tyrosine kinase signalling pathway. We show that the expression of Socs1 mRNA is rapidly increased in primary bone marrow-derived mast cells following exposure to Steel factor, and Socs1 inducibly binds to the Kit receptor tyrosine kinase via its Src homology 2 (SH2) domain. Previous studies have shown that Socs1 suppresses cytokine-mediated differentiation in M1 cells inhibiting Janus family kinases. In contrast, constitutive expression of Socs1 suppresses the mitogenic potential of Kit while maintaining Steel factor-dependent cell survival signals. Unlike Janus kinases, Socs1 does not inhibit the catalytic activity of the Kit tyrosine kinase. In order to define the mechanism by which Socs1-mediated suppression of Kit-dependent mitogenesis occurs, we demonstrate that Socs1 binds to the signalling proteins Grb-2 and the Rho-family guanine nucleotide exchange factors Vav. We show that Grb2 binds Socs1 via its SH3 domains to putative diproline determinants located in the N-terminus of Socs1, and Socs1 binds to the N-terminal regulatory region of Vav. These data suggest that Socs1 is an inducible switch which modulates proliferative signals in favour of cell survival signals and functions as an adaptor protein in receptor tyrosine kinase signalling pathways. (+info)

Interleukin-18 binding protein: a novel modulator of the Th1 cytokine response. (3/33104)

An interleukin-18 binding protein (IL-18BP) was purified from urine by chromatography on IL-18 beads, sequenced, cloned, and expressed in COS7 cells. IL-18BP abolished IL-18 induction of interferon-gamma (IFNgamma), IL-8, and activation of NF-kappaB in vitro. Administration of IL-18BP to mice abrogated circulating IFNgamma following LPS. Thus, IL-18BP functions as an inhibitor of the early Th1 cytokine response. IL-18BP is constitutively expressed in the spleen, belongs to the immunoglobulin superfamily, and has limited homology to the IL-1 type II receptor. Its gene was localized on human chromosome 11q13, and no exon coding for a transmembrane domain was found in an 8.3 kb genomic sequence. Several Poxviruses encode putative proteins highly homologous to IL-18BP, suggesting that viral products may attenuate IL-18 and interfere with the cytotoxic T cell response. (+info)

Differential regulation of vascular endothelial growth factor and its receptor fms-like-tyrosine kinase is mediated by nitric oxide in rat renal mesangial cells. (4/33104)

Under conditions associated with local and systemic inflammation, mesangial cells and invading immune cells are likely to be responsible for the release of large amounts of nitric oxide (NO) in the glomerulus. To further define the mechanisms of NO action in the glomerulus, we attempted to identify genes which are regulated by NO in rat glomerular mesangial cells. We identified vascular endothelial growth factor (VEGF) and its receptor fms-like tyrosine kinase (FLT-1) to be under the regulatory control of exogenously applied NO in these cells. Using S-nitroso-glutathione (GSNO) as an NO-donating agent, VEGF expression was strongly induced, whereas expression of its FLT-1 receptor simultaneously decreased. Expressional regulation of VEGF and FLT-1 mRNA was transient and occurred rapidly within 1-3 h after GSNO treatment. Expression of a second VEGF-specific receptor, fetal liver kinase-1 (FLK-1/KDR), could not be detected. The inflammatory cytokine interleukin-1beta mediated a moderate increase in VEGF expression after 24 h and had no influence on FLT-1 expression. In contrast, platelet-derived growth factor-BB and basic fibroblast growth factor had no effect on VEGF expression, but strongly induced FLT-1 mRNA levels. Obviously, there is a differential regulation of VEGF and its receptor FLT-1 by NO, cytokines and growth factors in rat mesangial cells. (+info)

Borrelia burgdorferi spirochetes induce mast cell activation and cytokine release. (5/33104)

The Lyme disease spirochete, Borrelia burgdorferi, is introduced into human hosts via tick bites. Among the cell types present in the skin which may initially contact spirochetes are mast cells. Since spirochetes are known to activate a variety of cell types in vitro, we tested whether B. burgdorferi spirochetes could activate mast cells. We report here that freshly isolated rat peritoneal mast cells or mouse MC/9 mast cells cultured in vitro with live or freeze-thawed B. burgdorferi spirochetes undergo low but detectable degranulation, as measured by [5-3H] hydroxytryptamine release, and they synthesize and secrete the proinflammatory cytokine tumor necrosis factor alpha (TNF-alpha). In contrast to findings in previous studies, where B. burgdorferi-associated activity was shown to be dependent upon protein lipidation, mast cell TNF-alpha release was not induced by either lipidated or unlipidated recombinant OspA. This activity was additionally shown to be protease sensitive and surface expressed. Finally, comparisons of TNF-alpha-inducing activity in known low-, intermediate-, and high-passage B. burgdorferi B31 isolates demonstrated passage-dependent loss of activity, indicating that the activity is probably plasmid encoded. These findings document the presence in low-passage B. burgdorferi spirochetes of a novel lipidation-independent activity capable of inducing cytokine release from host cells. (+info)

Potent immunoregulatory effects of Salmonella typhi flagella on antigenic stimulation of human peripheral blood mononuclear cells. (6/33104)

A key function of monocytes/macrophages (Mphi) is to present antigens to T cells. However, upon interaction with bacteria, Mphi lose their ability to effectively present soluble antigens. This functional loss was associated with alterations in the expression of adhesion molecules and CD14 and a reduction in the uptake of soluble antigen. Recently, we have demonstrated that Salmonella typhi flagella (STF) markedly decrease CD14 expression and are potent inducers of proinflammatory cytokine production by human peripheral blood mononuclear cells (hPBMC). In order to determine whether S. typhi and soluble STF also alter the ability of Mphi to activate T cells to proliferate to antigens and mitogens, hPBMC were cultured in the presence of tetanus toxoid (TT) or phytohemagglutinin (PHA) and either killed whole-cell S. typhi or purified STF protein. Both whole-cell S. typhi and STF suppressed proliferation to PHA and TT. This decreased proliferation was not a result of increased Mphi production of nitric oxide, prostaglandin E2, or oxygen radicals or the release of interleukin-1beta, tumor necrosis factor alpha, interleukin-6, or interleukin-10 following exposure to STF. However, the ability to take up soluble antigen, as determined by fluorescein isothiocyanate-labeled dextran uptake, was reduced in cells cultured with STF. Moreover, there was a dramatic reduction in the expression of CD54 on Mphi after exposure to STF. These results indicate that whole-cell S. typhi and STF have the ability to alter in vitro proliferation to soluble antigens and mitogens by affecting Mphi function. (+info)

Clearance of Chlamydia trachomatis from the murine genital mucosa does not require perforin-mediated cytolysis or Fas-mediated apoptosis. (7/33104)

The molecular mechanisms of resistance to genital infection with the mouse pneumonitis (MoPn) strain of Chlamydia trachomatis are unknown. A role for major histocompatibility complex class II-restricted, interleukin-12-dependent CD4(+) T cells has been established, but the functional activity of these cells does not depend on secretion of gamma interferon. Here we examined the potential contribution of T-cell-mediated cytotoxicity and apoptosis to mucosal clearance of MoPn by using mice deficient in the molecular mediators of target cell lysis. Animals lacking perforin, Fas, Fas ligand, or both perforin and Fas ligand were infected genitally with C. trachomatis MoPn and monitored for expression of immunity to chlamydial antigens and clearance of MoPn from the genital mucosa. In each case, the profile of spleen cytokine production, the magnitude of the host antibody response, and the kinetics of chlamydial clearance were similar to those of genetically intact controls. Compensatory overproduction of tumor necrosis factor alpha, an alternate mediator of apoptosis in certain cell types, did not appear to account for the ability of mutant mice to resolve Chlamydia infections. These results fail to support CD4(+) T-cell-mediated apoptosis or CD8(+) T-cell-mediated cytotoxicity as being critical to the clearance of C. trachomatis MoPn urogenital infections. (+info)

Effect of transforming growth factor beta on experimental Salmonella typhimurium infection in mice. (8/33104)

We have investigated the effect of the in vivo administration of recombinant transforming growth factor beta (rTGF-beta) on the pathogenic mechanisms involved in Salmonella typhimurium experimental infection in mice. The protective response elicited by macrophages was induced by rTGF-beta1 by 2 days after experimental infection, as demonstrated by an increased NO production, while the humoral protective effect began with cytokine mRNA expression 2 days after the challenge and continued after 5 days with cytokine release and lymphocyte activation. We demonstrated that all mice who received rTGF-beta1 survived 7 days after infection. The number of bacteria recovered in the spleens and in the livers of rTGF-beta1-treated mice 2 and 5 days after infection was significantly smaller than that found in the same organs after phosphate-buffered saline (PBS) inoculation. Furthermore, 2 and 5 days after infection, splenic macrophages from rTGF-beta1-treated mice showed a greater NO production than did those from PBS-treated mice. The effect of rTGF-beta1 on S. typhimurium infection in mice was correlated with the expression of cell costimulatory CD28 molecules. Five days after S. typhimurium infection, the percentage of CD28(+)-expressing T cells in splenic lymphocytes from rTGF-beta1-treated mice increased with respect to that from control mice. Gamma interferon (IFN-gamma) mRNA was present in a greater amount in spleen cells from rTGF-beta1-treated mice after 2 days, although the intensity of the band decreased 5 days after the challenge. A similar pattern was obtained with the mRNAs for interleukin-1alpha (IL-1alpha), IL-6, TGF-beta, and inducible nitric oxide synthase, which showed greater expression in cells obtained from rTGF-beta1-treated and S. typhimurium-infected mice 2 days after challenge. The treatment with rTGF-beta1 induced an increase in IL-1alpha and IFN-gamma release in the supernatant of splenocyte cultures 5 days after the experimental infection with S. typhimurium. Moreover, we demonstrated that 5 days after infection, the IFN-gamma titer was significantly greater in the sera of rTGF-beta-treated mice than in those of PBS-treated mice. Also, hsp60 showed greater expression 2 days after the challenge in splenocytes from rTGF-beta1-treated mice. The role played by proinflammatory and immunoregulatory cytokines and by CD28 is discussed. (+info)

There are several key features of inflammation:

1. Increased blood flow: Blood vessels in the affected area dilate, allowing more blood to flow into the tissue and bringing with it immune cells, nutrients, and other signaling molecules.
2. Leukocyte migration: White blood cells, such as neutrophils and monocytes, migrate towards the site of inflammation in response to chemical signals.
3. Release of mediators: Inflammatory mediators, such as cytokines and chemokines, are released by immune cells and other cells in the affected tissue. These molecules help to coordinate the immune response and attract more immune cells to the site of inflammation.
4. Activation of immune cells: Immune cells, such as macrophages and T cells, become activated and start to phagocytose (engulf) pathogens or damaged tissue.
5. Increased heat production: Inflammation can cause an increase in metabolic activity in the affected tissue, leading to increased heat production.
6. Redness and swelling: Increased blood flow and leakiness of blood vessels can cause redness and swelling in the affected area.
7. Pain: Inflammation can cause pain through the activation of nociceptors (pain-sensing neurons) and the release of pro-inflammatory mediators.

Inflammation can be acute or chronic. Acute inflammation is a short-term response to injury or infection, which helps to resolve the issue quickly. Chronic inflammation is a long-term response that can cause ongoing damage and diseases such as arthritis, asthma, and cancer.

There are several types of inflammation, including:

1. Acute inflammation: A short-term response to injury or infection.
2. Chronic inflammation: A long-term response that can cause ongoing damage and diseases.
3. Autoimmune inflammation: An inappropriate immune response against the body's own tissues.
4. Allergic inflammation: An immune response to a harmless substance, such as pollen or dust mites.
5. Parasitic inflammation: An immune response to parasites, such as worms or fungi.
6. Bacterial inflammation: An immune response to bacteria.
7. Viral inflammation: An immune response to viruses.
8. Fungal inflammation: An immune response to fungi.

There are several ways to reduce inflammation, including:

1. Medications such as nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, and disease-modifying anti-rheumatic drugs (DMARDs).
2. Lifestyle changes, such as a healthy diet, regular exercise, stress management, and getting enough sleep.
3. Alternative therapies, such as acupuncture, herbal supplements, and mind-body practices.
4. Addressing underlying conditions, such as hormonal imbalances, gut health issues, and chronic infections.
5. Using anti-inflammatory compounds found in certain foods, such as omega-3 fatty acids, turmeric, and ginger.

It's important to note that chronic inflammation can lead to a range of health problems, including:

1. Arthritis
2. Diabetes
3. Heart disease
4. Cancer
5. Alzheimer's disease
6. Parkinson's disease
7. Autoimmune disorders, such as lupus and rheumatoid arthritis.

Therefore, it's important to manage inflammation effectively to prevent these complications and improve overall health and well-being.

1) They share similarities with humans: Many animal species share similar biological and physiological characteristics with humans, making them useful for studying human diseases. For example, mice and rats are often used to study diseases such as diabetes, heart disease, and cancer because they have similar metabolic and cardiovascular systems to humans.

2) They can be genetically manipulated: Animal disease models can be genetically engineered to develop specific diseases or to model human genetic disorders. This allows researchers to study the progression of the disease and test potential treatments in a controlled environment.

3) They can be used to test drugs and therapies: Before new drugs or therapies are tested in humans, they are often first tested in animal models of disease. This allows researchers to assess the safety and efficacy of the treatment before moving on to human clinical trials.

4) They can provide insights into disease mechanisms: Studying disease models in animals can provide valuable insights into the underlying mechanisms of a particular disease. This information can then be used to develop new treatments or improve existing ones.

5) Reduces the need for human testing: Using animal disease models reduces the need for human testing, which can be time-consuming, expensive, and ethically challenging. However, it is important to note that animal models are not perfect substitutes for human subjects, and results obtained from animal studies may not always translate to humans.

6) They can be used to study infectious diseases: Animal disease models can be used to study infectious diseases such as HIV, TB, and malaria. These models allow researchers to understand how the disease is transmitted, how it progresses, and how it responds to treatment.

7) They can be used to study complex diseases: Animal disease models can be used to study complex diseases such as cancer, diabetes, and heart disease. These models allow researchers to understand the underlying mechanisms of the disease and test potential treatments.

8) They are cost-effective: Animal disease models are often less expensive than human clinical trials, making them a cost-effective way to conduct research.

9) They can be used to study drug delivery: Animal disease models can be used to study drug delivery and pharmacokinetics, which is important for developing new drugs and drug delivery systems.

10) They can be used to study aging: Animal disease models can be used to study the aging process and age-related diseases such as Alzheimer's and Parkinson's. This allows researchers to understand how aging contributes to disease and develop potential treatments.

There are several symptoms of RA, including:

1. Joint pain and stiffness, especially in the hands and feet
2. Swollen and warm joints
3. Redness and tenderness in the affected areas
4. Fatigue, fever, and loss of appetite
5. Loss of range of motion in the affected joints
6. Firm bumps of tissue under the skin (rheumatoid nodules)

RA can be diagnosed through a combination of physical examination, medical history, blood tests, and imaging studies such as X-rays or ultrasound. Treatment typically involves a combination of medications, including nonsteroidal anti-inflammatory drugs (NSAIDs), disease-modifying anti-rheumatic drugs (DMARDs), and biologic agents. Lifestyle modifications such as exercise and physical therapy can also be helpful in managing symptoms and improving quality of life.

There is no cure for RA, but early diagnosis and aggressive treatment can help to slow the progression of the disease and reduce symptoms. With proper management, many people with RA are able to lead active and fulfilling lives.

Examples of autoimmune diseases include:

1. Rheumatoid arthritis (RA): A condition where the immune system attacks the joints, leading to inflammation, pain, and joint damage.
2. Lupus: A condition where the immune system attacks various body parts, including the skin, joints, and organs.
3. Hashimoto's thyroiditis: A condition where the immune system attacks the thyroid gland, leading to hypothyroidism.
4. Multiple sclerosis (MS): A condition where the immune system attacks the protective covering of nerve fibers in the central nervous system, leading to communication problems between the brain and the rest of the body.
5. Type 1 diabetes: A condition where the immune system attacks the insulin-producing cells in the pancreas, leading to high blood sugar levels.
6. Guillain-Barré syndrome: A condition where the immune system attacks the nerves, leading to muscle weakness and paralysis.
7. Psoriasis: A condition where the immune system attacks the skin, leading to red, scaly patches.
8. Crohn's disease and ulcerative colitis: Conditions where the immune system attacks the digestive tract, leading to inflammation and damage to the gut.
9. Sjögren's syndrome: A condition where the immune system attacks the glands that produce tears and saliva, leading to dry eyes and mouth.
10. Vasculitis: A condition where the immune system attacks the blood vessels, leading to inflammation and damage to the blood vessels.

The symptoms of autoimmune diseases vary depending on the specific disease and the organs or tissues affected. Common symptoms include fatigue, fever, joint pain, skin rashes, and swollen lymph nodes. Treatment for autoimmune diseases typically involves medication to suppress the immune system and reduce inflammation, as well as lifestyle changes such as dietary changes and stress management techniques.

Psoriasis can affect any part of the body, including the scalp, elbows, knees, and lower back. The symptoms of psoriasis can vary in severity, and the condition can have a significant impact on quality of life. In addition to physical discomfort, psoriasis can also cause emotional distress and stigma.

There is no cure for psoriasis, but there are several treatment options available, including topical creams and ointments, light therapy, and systemic medications such as biologic drugs. With proper treatment, many people with psoriasis are able to manage their symptoms and improve their quality of life.

Psoriasis is relatively common, affecting approximately 2-3% of the global population, with a higher prevalence in Caucasians than in other races. It can occur at any age, but typically starts in the late teenage years or early adulthood. Psoriasis is often associated with other health conditions, such as diabetes, heart disease, and depression.

Overall, psoriasis is a complex and multifactorial condition that requires a comprehensive approach to management, including both physical and emotional support. With appropriate treatment and self-care, people with psoriasis can lead full and active lives.

The term "acute-phase" describes the rapid onset and short duration of this reaction, which typically lasts for hours to days before resolving as the body's inflammatory response subsides. APR is characterized by a series of molecular events that result in altered expression of genes involved in inflammation, immune response, and tissue repair.

Some key components of an acute-phase reaction include:

1. Cytokine production: Cytokines are signaling molecules released by immune cells, such as white blood cells, that coordinate the immune response. During an APR, cytokine levels increase, triggering a cascade of downstream effects.
2. Leukocyte trafficking: White blood cells migrate towards sites of inflammation or infection, where they phagocytose (engulf and digest) pathogens and cellular debris. This process helps to limit the spread of infection and initiate tissue repair.
3. Coagulation cascade: The APR triggers a complex series of events involving blood coagulation factors, leading to the formation of blood clots and preventing excessive bleeding.
4. Anti-inflammatory response: As the APR progresses, anti-inflammatory cytokines, such as interleukin-10 (IL-10), are produced to dampen the inflammatory response and promote tissue repair.
5. Cellular proliferation: To replace damaged cells and tissues, the APR stimulates cellular proliferation and tissue regeneration.
6. Nutrient mobilization: The APR enhances nutrient uptake and utilization by immune cells, allowing them to mount an effective response to the stress.
7. Hormonal changes: The APR is accompanied by changes in hormone levels, such as the increase in corticotropin-releasing factor (CRF) and cortisol, which help to mobilize energy resources and regulate metabolism.
8. Immune tolerance: The APR helps to establish immune tolerance, preventing excessive or inappropriate immune responses that can lead to autoimmune diseases or allergies.
9. Tissue remodeling: The APR stimulates the remodeling of damaged tissues, allowing for the restoration of normal tissue function.
10. Memory formation: The APR sets the stage for the formation of immunological memory, which enables the immune system to mount a more effective response to future infections or stressors.

Here are some key points to define sepsis:

1. Inflammatory response: Sepsis is characterized by an excessive and uncontrolled inflammatory response to an infection. This can lead to tissue damage and organ dysfunction.
2. Systemic symptoms: Patients with sepsis often have systemic symptoms such as fever, chills, rapid heart rate, and confusion. They may also experience nausea, vomiting, and diarrhea.
3. Organ dysfunction: Sepsis can cause dysfunction in multiple organs, including the lungs, kidneys, liver, and heart. This can lead to organ failure and death if not treated promptly.
4. Infection source: Sepsis is usually caused by a bacterial infection, but it can also be caused by fungal or viral infections. The infection can be localized or widespread, and it can affect different parts of the body.
5. Severe sepsis: Severe sepsis is a more severe form of sepsis that is characterized by severe organ dysfunction and a higher risk of death. Patients with severe sepsis may require intensive care unit (ICU) admission and mechanical ventilation.
6. Septic shock: Septic shock is a life-threatening condition that occurs when there is severe circulatory dysfunction due to sepsis. It is characterized by hypotension, vasopressor use, and organ failure.

Early recognition and treatment of sepsis are critical to preventing serious complications and improving outcomes. The Sepsis-3 definition is widely used in clinical practice to diagnose sepsis and severe sepsis.

There are several types of hypersensitivity reactions, including:

1. Type I hypersensitivity: This is also known as immediate hypersensitivity and occurs within minutes to hours after exposure to the allergen. It is characterized by the release of histamine and other chemical mediators from immune cells, leading to symptoms such as hives, itching, swelling, and difficulty breathing. Examples of Type I hypersensitivity reactions include allergies to pollen, dust mites, or certain foods.
2. Type II hypersensitivity: This is also known as cytotoxic hypersensitivity and occurs within days to weeks after exposure to the allergen. It is characterized by the immune system producing antibodies against specific proteins on the surface of cells, leading to their destruction. Examples of Type II hypersensitivity reactions include blood transfusion reactions and serum sickness.
3. Type III hypersensitivity: This is also known as immune complex hypersensitivity and occurs when antigens bind to immune complexes, leading to the formation of deposits in tissues. Examples of Type III hypersensitivity reactions include rheumatoid arthritis and systemic lupus erythematosus.
4. Type IV hypersensitivity: This is also known as delayed-type hypersensitivity and occurs within weeks to months after exposure to the allergen. It is characterized by the activation of T cells, leading to inflammation and tissue damage. Examples of Type IV hypersensitivity reactions include contact dermatitis and toxic epidermal necrolysis.

The diagnosis of hypersensitivity often involves a combination of medical history, physical examination, laboratory tests, and elimination diets or challenges. Treatment depends on the specific type of hypersensitivity reaction and may include avoidance of the allergen, medications such as antihistamines or corticosteroids, and immunomodulatory therapy.

These animal models allow researchers to study the underlying causes of arthritis, test new treatments and therapies, and evaluate their effectiveness in a controlled environment before moving to human clinical trials. Experimental arthritis models are used to investigate various aspects of the disease, including its pathophysiology, immunogenicity, and potential therapeutic targets.

Some common experimental arthritis models include:

1. Collagen-induced arthritis (CIA): This model is induced in mice by immunizing them with type II collagen, which leads to an autoimmune response and inflammation in the joints.
2. Rheumatoid arthritis (RA) models: These models are developed by transferring cells from RA patients into immunodeficient mice, which then develop arthritis-like symptoms.
3. Osteoarthritis (OA) models: These models are induced in animals by subjecting them to joint injury or overuse, which leads to degenerative changes in the joints and bone.
4. Psoriatic arthritis (PsA) models: These models are developed by inducing psoriasis in mice, which then develop arthritis-like symptoms.

Experimental arthritis models have contributed significantly to our understanding of the disease and have helped to identify potential therapeutic targets for the treatment of arthritis. However, it is important to note that these models are not perfect representations of human arthritis and should be used as tools to complement, rather than replace, human clinical trials.

The most common type of colitis is ulcerative colitis, which affects the rectum and lower part of the colon. The symptoms of ulcerative colitis can include:

* Diarrhea (which may be bloody)
* Abdominal pain and cramping
* Rectal bleeding
* Weight loss
* Fever
* Loss of appetite
* Nausea and vomiting

Microscopic colitis is another type of colitis that is characterized by inflammation in the colon, but without visible ulcers or bleeding. The symptoms of microscopic colitis are similar to those of ulcerative colitis, but may be less severe.

Other types of colitis include:

* Infantile colitis: This is a rare condition that affects babies and young children, and is characterized by diarrhea, fever, and vomiting.
* Isomorphic colitis: This is a rare condition that affects the colon and rectum, and is characterized by inflammation and symptoms similar to ulcerative colitis.
* Radiation colitis: This is a condition that occurs after radiation therapy to the pelvic area, and is characterized by inflammation and symptoms similar to ulcerative colitis.
* Ischemic colitis: This is a condition where there is a reduction in blood flow to the colon, which can lead to inflammation and symptoms such as abdominal pain and diarrhea.

The diagnosis of colitis typically involves a combination of physical examination, medical history, and diagnostic tests such as:

* Colonoscopy: This is a test that uses a flexible tube with a camera on the end to visualize the inside of the colon and rectum.
* Endoscopy: This is a test that uses a flexible tube with a camera on the end to visualize the inside of the esophagus, stomach, and duodenum.
* Stool tests: These are tests that analyze stool samples for signs of inflammation or infection.
* Blood tests: These are tests that analyze blood samples for signs of inflammation or infection.
* Biopsy: This is a test that involves taking a small sample of tissue from the colon and examining it under a microscope for signs of inflammation or infection.

Treatment for colitis depends on the underlying cause, but may include medications such as:

* Aminosalicylates: These are medications that help to reduce inflammation in the colon and relieve symptoms such as diarrhea and abdominal pain. Examples include sulfasalazine (Azulfidine) and mesalamine (Asacol).
* Corticosteroids: These are medications that help to reduce inflammation in the body. They may be used short-term to control acute flares of colitis, or long-term to maintain remission. Examples include prednisone and hydrocortisone.
* Immunomodulators: These are medications that help to suppress the immune system and reduce inflammation. Examples include azathioprine (Imuran) and mercaptopurine (Purinethol).
* Biologics: These are medications that target specific proteins involved in the inflammatory response. Examples include infliximab (Remicade) and adalimumab (Humira).

In addition to medication, lifestyle changes such as dietary modifications and stress management techniques may also be helpful in managing colitis symptoms. Surgery may be necessary in some cases where the colitis is severe or persistent, and involves removing damaged portions of the colon and rectum.

It's important to note that colitis can increase the risk of developing colon cancer, so regular screening for colon cancer is recommended for people with chronic colitis. Additionally, people with colitis may be more susceptible to other health problems such as osteoporosis, osteopenia, and liver disease, so it's important to work closely with a healthcare provider to monitor for these conditions and take steps to prevent them.

Shock refers to a severe and sudden drop in blood pressure, which can lead to inadequate perfusion of vital organs such as the brain, heart, and lungs. There are several types of shock, including hypovolemic shock (caused by bleeding or dehydration), septic shock (caused by an overwhelming bacterial infection), and cardiogenic shock (caused by a heart attack or other cardiac condition).

Septic refers to the presence of bacteria or other microorganisms in the bloodstream, which can cause a range of symptoms including fever, chills, and confusion. Sepsis is a serious and potentially life-threatening condition that can lead to organ failure and death if left untreated.

Septic shock is a specific type of shock that occurs as a result of sepsis, which is the body's systemic inflammatory response to an infection. Septic shock is characterized by severe vasopressor (a medication used to increase blood pressure) and hypotension (low blood pressure), and it can lead to multiple organ failure and death if not treated promptly and effectively.

In summary, shock refers to a drop in blood pressure, while septic refers to the presence of bacteria or other microorganisms in the bloodstream. Septic shock is a specific type of shock that occurs as a result of sepsis, and it can be a life-threatening condition if not treated promptly and effectively.

Endotoxemia can occur in individuals who have a severe bacterial infection, such as pneumonia or meningitis, or those who have a prosthetic device or other foreign body that becomes infected with gram-negative bacteria. Treatment of endotoxemia typically involves antibiotics and supportive care to manage symptoms and prevent further complications. In severe cases, medications such as corticosteroids and vasopressors may be used to help reduce inflammation and improve blood flow.

Endotoxemia is a serious medical condition that requires prompt diagnosis and treatment to prevent complications and improve outcomes for patients.

Asthma can cause recurring episodes of wheezing, coughing, chest tightness, and shortness of breath. These symptoms occur when the muscles surrounding the airways contract, causing the airways to narrow and swell. This can be triggered by exposure to environmental allergens or irritants such as pollen, dust mites, pet dander, or respiratory infections.

There is no cure for asthma, but it can be managed with medication and lifestyle changes. Treatment typically includes inhaled corticosteroids to reduce inflammation, bronchodilators to open up the airways, and rescue medications to relieve symptoms during an asthma attack.

Asthma is a common condition that affects people of all ages, but it is most commonly diagnosed in children. According to the American Lung Association, more than 25 million Americans have asthma, and it is the third leading cause of hospitalization for children under the age of 18.

While there is no cure for asthma, early diagnosis and proper treatment can help manage symptoms and improve quality of life for those affected by the condition.

Examples of acute diseases include:

1. Common cold and flu
2. Pneumonia and bronchitis
3. Appendicitis and other abdominal emergencies
4. Heart attacks and strokes
5. Asthma attacks and allergic reactions
6. Skin infections and cellulitis
7. Urinary tract infections
8. Sinusitis and meningitis
9. Gastroenteritis and food poisoning
10. Sprains, strains, and fractures.

Acute diseases can be treated effectively with antibiotics, medications, or other therapies. However, if left untreated, they can lead to chronic conditions or complications that may require long-term care. Therefore, it is important to seek medical attention promptly if symptoms persist or worsen over time.

Symptoms of pneumonia may include cough, fever, chills, difficulty breathing, and chest pain. In severe cases, pneumonia can lead to respiratory failure, sepsis, and even death.

There are several types of pneumonia, including:

1. Community-acquired pneumonia (CAP): This type of pneumonia is caused by bacteria or viruses and typically affects healthy people outside of hospitals.
2. Hospital-acquired pneumonia (HAP): This type of pneumonia is caused by bacteria or fungi and typically affects people who are hospitalized for other illnesses or injuries.
3. Aspiration pneumonia: This type of pneumonia is caused by food, liquids, or other foreign matter being inhaled into the lungs.
4. Pneumocystis pneumonia (PCP): This type of pneumonia is caused by a fungus and typically affects people with weakened immune systems, such as those with HIV/AIDS.
5. Viral pneumonia: This type of pneumonia is caused by viruses and can be more common in children and young adults.

Pneumonia is typically diagnosed through a combination of physical examination, medical history, and diagnostic tests such as chest X-rays or blood tests. Treatment may involve antibiotics, oxygen therapy, and supportive care to manage symptoms and help the patient recover. In severe cases, hospitalization may be necessary to provide more intensive care and monitoring.

Prevention of pneumonia includes vaccination against certain types of bacteria and viruses, good hygiene practices such as frequent handwashing, and avoiding close contact with people who are sick. Early detection and treatment can help reduce the risk of complications and improve outcomes for those affected by pneumonia.

The burden of chronic diseases is significant, with over 70% of deaths worldwide attributed to them, according to the World Health Organization (WHO). In addition to the physical and emotional toll they take on individuals and their families, chronic diseases also pose a significant economic burden, accounting for a large proportion of healthcare expenditure.

In this article, we will explore the definition and impact of chronic diseases, as well as strategies for managing and living with them. We will also discuss the importance of early detection and prevention, as well as the role of healthcare providers in addressing the needs of individuals with chronic diseases.

What is a Chronic Disease?

A chronic disease is a condition that lasts for an extended period of time, often affecting daily life and activities. Unlike acute diseases, which have a specific beginning and end, chronic diseases are long-term and persistent. Examples of chronic diseases include:

1. Diabetes
2. Heart disease
3. Arthritis
4. Asthma
5. Cancer
6. Chronic obstructive pulmonary disease (COPD)
7. Chronic kidney disease (CKD)
8. Hypertension
9. Osteoporosis
10. Stroke

Impact of Chronic Diseases

The burden of chronic diseases is significant, with over 70% of deaths worldwide attributed to them, according to the WHO. In addition to the physical and emotional toll they take on individuals and their families, chronic diseases also pose a significant economic burden, accounting for a large proportion of healthcare expenditure.

Chronic diseases can also have a significant impact on an individual's quality of life, limiting their ability to participate in activities they enjoy and affecting their relationships with family and friends. Moreover, the financial burden of chronic diseases can lead to poverty and reduce economic productivity, thus having a broader societal impact.

Addressing Chronic Diseases

Given the significant burden of chronic diseases, it is essential that we address them effectively. This requires a multi-faceted approach that includes:

1. Lifestyle modifications: Encouraging healthy behaviors such as regular physical activity, a balanced diet, and smoking cessation can help prevent and manage chronic diseases.
2. Early detection and diagnosis: Identifying risk factors and detecting diseases early can help prevent or delay their progression.
3. Medication management: Effective medication management is crucial for controlling symptoms and slowing disease progression.
4. Multi-disciplinary care: Collaboration between healthcare providers, patients, and families is essential for managing chronic diseases.
5. Health promotion and disease prevention: Educating individuals about the risks of chronic diseases and promoting healthy behaviors can help prevent their onset.
6. Addressing social determinants of health: Social determinants such as poverty, education, and employment can have a significant impact on health outcomes. Addressing these factors is essential for reducing health disparities and improving overall health.
7. Investing in healthcare infrastructure: Investing in healthcare infrastructure, technology, and research is necessary to improve disease detection, diagnosis, and treatment.
8. Encouraging policy change: Policy changes can help create supportive environments for healthy behaviors and reduce the burden of chronic diseases.
9. Increasing public awareness: Raising public awareness about the risks and consequences of chronic diseases can help individuals make informed decisions about their health.
10. Providing support for caregivers: Chronic diseases can have a significant impact on family members and caregivers, so providing them with support is essential for improving overall health outcomes.

Conclusion

Chronic diseases are a major public health burden that affect millions of people worldwide. Addressing these diseases requires a multi-faceted approach that includes lifestyle changes, addressing social determinants of health, investing in healthcare infrastructure, encouraging policy change, increasing public awareness, and providing support for caregivers. By taking a comprehensive approach to chronic disease prevention and management, we can improve the health and well-being of individuals and communities worldwide.

The SIRS criteria were first established by the American Academy of Pediatrics in 1992 and have since been widely adopted by healthcare professionals around the world. These criteria include:

1. Body temperature >38°C (>100.4°F) or <36°C (<96.8°F)
2. Heart rate >90 beats per minute in infants <3 months old, or >100 beats per minute in infants >3 months old and children <12 years old, or >120 beats per minute in adolescents and adults
3. Respiratory rate >24 breaths per minute, or arterial CO2 tension (PaCO2) <32 mmHg
4. White blood cell count >12,000 cells/mm3, or band forms >10% of total white blood cells, or presence of bacteria in the blood or other bodily fluids
5. Clinical signs of infection, such as tachycardia, tachypnea, or signs of sepsis (e.g., altered mental status, confusion, or hypotension)

If a patient meets two or more of these criteria, they are considered to have SIRS. The diagnosis is based on the presence of an inflammatory response, rather than the specific cause of the response.

The management of SIRS involves identifying and treating the underlying cause of the inflammation, as well as providing supportive care to address any complications that may have arisen. This can include antibiotics for bacterial infections, fluid resuscitation to maintain blood pressure and hydration, and oxygen therapy to improve oxygenation of the body's tissues. In severe cases, hospitalization may be necessary to provide more intensive care and monitoring.

It is important to note that SIRS can progress to sepsis if left untreated or if the underlying infection is not effectively managed. Sepsis is a life-threatening condition that can lead to organ failure and death. Therefore, it is crucial to identify and treat SIRS promptly and effectively to prevent progression to sepsis.

The exact cause of osteoarthritis is not known, but it is thought to be due to a combination of factors such as genetics, wear and tear on joints over time, and injuries or trauma to the joint. Osteoarthritis can affect any joint in the body, but it most commonly affects the hands, knees, hips, and spine.

The symptoms of osteoarthritis can vary depending on the severity of the condition and which joint is affected. Common symptoms include:

* Pain or tenderness in the joint
* Stiffness, especially after periods of rest or inactivity
* Limited mobility or loss of flexibility
* Grating or crackling sensations when the joint is moved
* Swelling or redness in the affected joint
* Muscle weakness or wasting

There is no cure for osteoarthritis, but there are several treatment options available to manage the symptoms and slow the progression of the disease. These include:

* Pain relief medications such as acetaminophen or nonsteroidal anti-inflammatory drugs (NSAIDs)
* Physical therapy to improve mobility and strength
* Lifestyle modifications such as weight loss, regular exercise, and avoiding activities that exacerbate the condition
* Bracing or orthotics to support the affected joint
* Corticosteroid injections or hyaluronic acid injections to reduce inflammation and improve joint function
* Joint replacement surgery in severe cases where other treatments have failed.

Early diagnosis and treatment of osteoarthritis can help manage symptoms, slow the progression of the disease, and improve quality of life for individuals with this condition.

There are several types of disease susceptibility, including:

1. Genetic predisposition: This refers to the inherent tendency of an individual to develop a particular disease due to their genetic makeup. For example, some families may have a higher risk of developing certain diseases such as cancer or heart disease due to inherited genetic mutations.
2. Environmental susceptibility: This refers to the increased risk of developing a disease due to exposure to environmental factors such as pollutants, toxins, or infectious agents. For example, someone who lives in an area with high levels of air pollution may be more susceptible to developing respiratory problems.
3. Lifestyle susceptibility: This refers to the increased risk of developing a disease due to unhealthy lifestyle choices such as smoking, lack of exercise, or poor diet. For example, someone who smokes and is overweight may be more susceptible to developing heart disease or lung cancer.
4. Immune system susceptibility: This refers to the increased risk of developing a disease due to an impaired immune system. For example, people with autoimmune disorders such as HIV/AIDS or rheumatoid arthritis may be more susceptible to opportunistic infections.

Understanding disease susceptibility can help healthcare providers identify individuals who are at risk of developing certain diseases and provide preventive measures or early intervention to reduce the risk of disease progression. Additionally, genetic testing can help identify individuals with a high risk of developing certain diseases, allowing for earlier diagnosis and treatment.

In summary, disease susceptibility refers to the predisposition of an individual to develop a particular disease or condition due to various factors such as genetics, environment, lifestyle choices, and immune system function. Understanding disease susceptibility can help healthcare providers identify individuals at risk and provide appropriate preventive measures or early intervention to reduce the risk of disease progression.

Disease progression can be classified into several types based on the pattern of worsening:

1. Chronic progressive disease: In this type, the disease worsens steadily over time, with a gradual increase in symptoms and decline in function. Examples include rheumatoid arthritis, osteoarthritis, and Parkinson's disease.
2. Acute progressive disease: This type of disease worsens rapidly over a short period, often followed by periods of stability. Examples include sepsis, acute myocardial infarction (heart attack), and stroke.
3. Cyclical disease: In this type, the disease follows a cycle of worsening and improvement, with periodic exacerbations and remissions. Examples include multiple sclerosis, lupus, and rheumatoid arthritis.
4. Recurrent disease: This type is characterized by episodes of worsening followed by periods of recovery. Examples include migraine headaches, asthma, and appendicitis.
5. Catastrophic disease: In this type, the disease progresses rapidly and unpredictably, with a poor prognosis. Examples include cancer, AIDS, and organ failure.

Disease progression can be influenced by various factors, including:

1. Genetics: Some diseases are inherited and may have a predetermined course of progression.
2. Lifestyle: Factors such as smoking, lack of exercise, and poor diet can contribute to disease progression.
3. Environmental factors: Exposure to toxins, allergens, and other environmental stressors can influence disease progression.
4. Medical treatment: The effectiveness of medical treatment can impact disease progression, either by slowing or halting the disease process or by causing unintended side effects.
5. Co-morbidities: The presence of multiple diseases or conditions can interact and affect each other's progression.

Understanding the type and factors influencing disease progression is essential for developing effective treatment plans and improving patient outcomes.

The disease is typically induced in laboratory animals such as mice or rats by immunizing them with myelin proteins, such as myelin basic protein (MBP) or proteolipid protein (PLP), emulsified in adjuvants. The resulting immune response leads to the production of autoantibodies and activated T cells that cross the blood-brain barrier and attack the CNS.

EAE is used as a model for MS because it shares many similarities with the human disease, including:

1. Demyelination: EAE induces demyelination of nerve fibers in the CNS, which is also a hallmark of MS.
2. Autoimmune response: The immune response in EAE is triggered by autoantigens, similar to MS.
3. Chronic course: EAE is a chronic disease with recurrent relapses, similar to MS.
4. Lesion distribution: EAE lesions are distributed throughout the CNS, including the cerebral cortex, cerebellum, brainstem, and spinal cord, which is also true for MS.

EAE has been used extensively in the study of MS to investigate the immunopathogenesis of the disease, to develop new diagnostic markers and treatments, and to test the efficacy of potential therapeutic agents.

Also known as eczema or atopic eczema.

Dermatitis, Atopic is a common condition that affects people of all ages but is most prevalent in children. It is often associated with other atopic conditions such as asthma and allergies. The exact cause of dermatitis, atopic is not known, but it is thought to involve a combination of genetic and environmental factors.

Symptoms of Dermatitis, Atopic:

* Redness and dryness of the skin
* Scaling and flaking of the skin
* Itching and burning sensations
* Thickening and pigmentation of the skin
* Small blisters or weeping sores

Atopic dermatitis can occur anywhere on the body but is most commonly found on the face, neck, hands, and feet.

Treatment for Dermatitis, Atopic:

* Moisturizers to keep the skin hydrated and reduce dryness
* Topical corticosteroids to reduce inflammation
* Antihistamines to relieve itching
* Phototherapy with ultraviolet light
* Oral immunomodulators for severe cases

It is important to note that dermatitis, atopic is a chronic condition, and treatment should be ongoing. Flare-ups may occur, and adjustments to the treatment plan may be necessary.

Prevention of Dermatitis, Atopic:

* Avoiding triggers such as soaps, detergents, and stress
* Keeping the skin well-moisturized
* Avoiding extreme temperatures and humidity
* Wearing soft, breathable clothing
* Using mild cleansers and avoiding harsh chemicals

Early diagnosis and treatment of dermatitis, atopic can help improve the quality of life for those affected. It is important to work with a healthcare professional to develop an appropriate treatment plan and manage symptoms effectively.

Respiratory hypersensitivity can be diagnosed through medical history, physical examination, and allergy testing. Treatment options include avoidance of allergens, medication, such as antihistamines or corticosteroids, and immunotherapy, which involves exposing the person to small amounts of the allergen over time to build up their tolerance.

Some people with respiratory hypersensitivity may experience more severe symptoms, such as asthma, which can be life-threatening if left untreated. It is important for individuals with respiratory hypersensitivity to work closely with their healthcare provider to manage their condition and prevent complications.

The symptoms of myocarditis can vary depending on the severity of the inflammation and the location of the affected areas of the heart muscle. Common symptoms include chest pain, shortness of breath, fatigue, and swelling in the legs and feet.

Myocarditis can be difficult to diagnose, as its symptoms are similar to those of other conditions such as coronary artery disease or heart failure. Diagnosis is typically made through a combination of physical examination, medical history, and results of diagnostic tests such as electrocardiogram (ECG), echocardiogram, and blood tests.

Treatment of myocarditis depends on the underlying cause and severity of the condition. Mild cases may require only rest and over-the-counter pain medication, while more severe cases may require hospitalization and intravenous medications to manage inflammation and cardiac function. In some cases, surgery may be necessary to repair or replace damaged heart tissue.

Prevention of myocarditis is important, as it can lead to serious complications such as heart failure and arrhythmias if left untreated. Prevention strategies include avoiding exposure to viruses and other infections, managing underlying medical conditions such as diabetes and high blood pressure, and getting regular check-ups with a healthcare provider to monitor cardiac function.

In summary, myocarditis is an inflammatory condition that affects the heart muscle, causing symptoms such as chest pain, shortness of breath, and fatigue. Diagnosis can be challenging, but treatment options range from rest and medication to hospitalization and surgery. Prevention is key to avoiding serious complications and maintaining good cardiac health.

There are several types of dermatitis, including:

1. Atopic dermatitis: a chronic condition characterized by dry, itchy skin and a tendency to develop allergies.
2. Contact dermatitis: a localized reaction to an allergen or irritant that comes into contact with the skin.
3. Seborrheic dermatitis: a condition characterized by redness, itching, and flaking skin on the scalp, face, or body.
4. Psoriasis: a chronic condition characterized by thick, scaly patches on the skin.
5. Cutaneous lupus erythematosus: a chronic autoimmune disorder that can cause skin rashes and lesions.
6. Dermatitis herpetiformis: a rare condition characterized by itchy blisters or rashes on the skin.

Dermatitis can be diagnosed through a physical examination, medical history, and sometimes laboratory tests such as patch testing or biopsy. Treatment options for dermatitis depend on the cause and severity of the condition, but may include topical creams or ointments, oral medications, phototherapy, or lifestyle changes such as avoiding allergens or irritants.

Wikimedia Commons has media related to Cytokines. Cytokine Signalling Forum Cytokine Tutorial Cytokine Gene Summary, Ontology, ... Over-secretion of cytokines can trigger a dangerous cytokine storm syndrome. Cytokine storms may have been the cause of severe ... with dramatic increases in cytokine levels. Another example of cytokine storm is seen in acute pancreatitis. Cytokines are ... Cytokines are peptides and cannot cross the lipid bilayer of cells to enter the cytoplasm. Cytokines have been shown to be ...

https://en.wikipedia.org/wiki/Cytokine

... s are receptors that bind to cytokines. In recent years, the cytokine receptors have come to demand the ... Soluble cytokine receptors are extremely common regulators of cytokine function. Soluble cytokine receptors typically consist ... PMID 9715251.[permanent dead link] Cytokine-cytokine receptor interaction map from KEGG Cytokine+receptors at the US National ... A classification of cytokine receptors based on their three-dimensional structure has been attempted. (Such a classification, ...

https://en.wikipedia.org/wiki/Cytokine_receptor

Cytokine is a monthly peer-reviewed academic journal covering the study of cytokines as they relate to multiple disciplines, ... It is the official journal of the International Cytokine & Interferon Society. The editor-in-chief is Dhan Kalvakolanu ( ... "Cytokine". 2016 Journal Citation Reports. Web of Science (Science ed.). Clarivate Analytics. 2017. Official website v t e ( ...

https://en.wikipedia.org/wiki/Cytokine_(journal)

An inflammatory cytokine or proinflammatory cytokine is a type of signaling molecule (a cytokine) that is secreted from immune ... An inflammatory cytokine is a type of cytokine (a signaling molecule) that is secreted from immune cells and certain other cell ... Some inflammatory cytokines have additional roles such as acting as growth factors. Pro-inflammatory cytokines such as IL-1β, ... Excessive amounts of proinflammatory cytokines have been shown to cause detrimental effects A proinflammatory cytokine affects ...

https://en.wikipedia.org/wiki/Inflammatory_cytokine

... is associated with the term cytokine pleiotropy, which refers to the ability of cytokines to exert multiple ... Cytokine redundancy is a term in immunology referring to the phenomenon in which, and the ability of, multiple cytokines to ... Ozaki, K; Leonard, WJ (16 August 2002). "Cytokine and cytokine receptor pleiotropy and redundancy". The Journal of Biological ... Nicola, NA (1994). "Cytokine pleiotropy and redundancy: a view from the receptor". Stem Cells. 12 Suppl 1: 3-12, discussion 12- ...

https://en.wikipedia.org/wiki/Cytokine_redundancy

... syndrome is a diverse set of conditions that can result in a cytokine storm. Cytokine storm syndromes include ... cytokine release syndrome and sepsis. The term "cytokine storm" is often loosely used interchangeably with cytokine release ... Human deaths from the bird flu H5N1 usually involve cytokine storms as well. Cytokine storm has also been implicated in ... During the COVID-19 pandemic, some doctors have attributed many deaths to cytokine storms. A cytokine storm can cause the ...

https://en.wikipedia.org/wiki/Cytokine_storm

Immediate-onset CRS is a cytokine storm, although severe cases of CRS have also been called cytokine storms. Symptoms include ... August 2010). "In vitro cytokine release assays for predicting cytokine release syndrome: the current state-of-the-science. ... inflammatory cytokines binding their cognate receptor on immune cells results in activation and stimulation of further cytokine ... Many of the cytokines elevated in CRS are not produced by CAR-T cells, but by myeloid cells that are pathogenically licensed ...

https://en.wikipedia.org/wiki/Cytokine_release_syndrome

Cytokine-adsorbing columns remove inflammatory toxins from the body. Such technology is currently being studied in more than 53 ... When cytokine-adsorbing columns are used in patients with septic shock, their additional clearance of antibiotics and ... Using cytokine-adsorbing columns involves channeling the patient's blood through a cartridge containing millions of minuscule ...

https://en.wikipedia.org/wiki/Cytokine_adsorbing_column

Cytokines are advantageous due to their small sizes, which allow them to reach intracellular targets. PEG binding to cytokines ... This causes the cytokine to be inactive in circulation, limiting systemic toxicity. The cytokine is activated upon binding to ... Conjugating cytokines to liposomal surfaces is a useful approach because it allows cytokines to bind to their respective target ... Antibody conjugation to cytokines can be used to improve site-specific delivery and prolong the cytokine half-life. ...

https://en.wikipedia.org/wiki/Cytokine_delivery_systems

... (also protein C17) is a protein that in humans is encoded by the CYTL1 gene. Protein C17 is a cytokine- ... "Entrez Gene: Cytokine-like 1". Liu X, Rapp N, Deans R, Cheng L (May 2000). "Molecular cloning and chromosomal mapping of a ... Ai Z, Jing W, Fang L (2016). "Cytokine-Like Protein 1(Cytl1): A Potential Molecular Mediator in Embryo Implantation". PLOS ONE ... candidate cytokine gene selectively expressed in human CD34+ cells". Genomics. 65 (3): 283-92. doi:10.1006/geno.2000.6170. PMID ...

https://en.wikipedia.org/wiki/Cytokine-like_protein_1

These NK cells referred to as cytokine induced memory-like natural killer cells are induced using cytokines, most commonly a ... They were given the name "cytokine-induced killer" because cultivation with certain cytokines is mandatory for the maturation ... Rosato Antonio, Sommaggio Roberta (Aug 2017). "Cytokines for the induction of antitumor effectors: The paradigm of Cytokine- ... Rosato Antonio, Sommaggio Roberta (Aug 2017). "Cytokines for the induction of antitumor effectors: The paradigm of Cytokine- ...

https://en.wikipedia.org/wiki/Cytokine-induced_killer_cell

... s are transmembrane receptors expressed on the surface of cells that recognize and respond to cytokines ... Members of the type I cytokine receptor family comprise different chains, some of which are involved in ligand/cytokine ... The common cytokine-binding domain is related to the Fibronectin type III domain. The signal transducing chains are often ... Cytokine+Receptors at the US National Library of Medicine Medical Subject Headings (MeSH) (Articles with short description, ...

https://en.wikipedia.org/wiki/Type_I_cytokine_receptor

The first protein to be classified as a suppressor of cytokine signaling, CIS (cytokine-inducible SH2), was discovered in 1995 ... Suppressor+of+Cytokine+Signaling+Proteins at the US National Library of Medicine Medical Subject Headings (MeSH) v t e (Cell ... SOCS (suppressor of cytokine signaling proteins) refers to a family of genes involved in inhibiting the JAK-STAT signaling ... SOCS have also been implicated in the regulation of cytokines, growth factors, and tumor suppression. It has been suggested ...

https://en.wikipedia.org/wiki/Suppressor_of_cytokine_signalling

"About Us". International Cytokine & Interferon Society. Retrieved 2020-05-12. "Cytokine". Elsevier. Cytokine & Interferon. ... The ICIS manages Cytokine, a peer-reviewed scientific journal covering all aspects of cytokine biology. The journal was ... The International Cytokine & Interferon Society (ICIS) is a non-profit organization composed of researchers of cytokines, ... As the premier organization in the field of cytokine biology, it has more than 950 member scientists. Katherine A. Fitzgerald ...

https://en.wikipedia.org/wiki/International_Cytokine_&_Interferon_Society

... s, also commonly known as class II cytokine receptors, are transmembrane proteins that are expressed ... Type II cytokine receptors are tyrosine-kinase-linked receptors. The intracellular domain of type II cytokine receptors is ... Class II cytokine receptors bind type I, type II, and type III interferons. Type I interferons play important roles in both the ... Typically type II cytokine receptors are heterodimers or multimers with a high and a low affinity component. These receptors ...

https://en.wikipedia.org/wiki/Type_II_cytokine_receptor

... is a protein that in humans is encoded by the CLNK gene. MIST is a member of the ... "Entrez Gene: Cytokine dependent hematopoietic cell linker". Retrieved 2017-09-06. Cronin S, Tomik B, Bradley DG, Slowik A, ...

https://en.wikipedia.org/wiki/Cytokine_dependent_hematopoietic_cell_linker

SSI family members are cytokine-inducible negative regulators of cytokine signaling. The expression of this gene can be induced ... Suppressor of cytokine signaling 1 is a protein that in humans is encoded by the SOCS1 gene. SOCS1 orthologs have been ... The suppressor of cytokine signaling 1 has been shown to interact with: Tax, CD117, Colony stimulating factor 1 receptor Growth ... Yoshimura A, Ohkubo T, Kiguchi T, Jenkins NA, Gilbert DJ, Copeland NG, Hara T, Miyajima A (June 1995). "A novel cytokine- ...

https://en.wikipedia.org/wiki/Suppressor_of_cytokine_signaling_1

... is a small cytokine that belongs to the CC chemokine subfamily. CCL4 is being secreted under mitogenic signals and ... January 1992). "Nucleotide sequence of the third cytokine LD78 gene and mapping of all three LD78 gene loci to human chromosome ... Napolitano M, Modi WS, Cevario SJ, Gnarra JR, Seuanez HN, Leonard WJ (September 1991). "The gene encoding the Act-2 cytokine. ... Chang HC, Reinherz EL (June 1989). "Isolation and characterization of a cDNA encoding a putative cytokine which is induced by ...

https://en.wikipedia.org/wiki/CCL4

Dinarello CA (2001). "IL-1α". In Durum SK, Oppenheim JJ, Feldmann M (eds.). Cytokine reference: a compendium of cytokines and ... Feldmann M, Saklatvala J (2001). "Proinflammatory cytokines". In Durum SK, Oppenheim JJ, Feldmann M (eds.). Cytokine reference ... "TLR-signaling and proinflammatory cytokines as drivers of tumorigenesis". Cytokine. 89: 127-135. doi:10.1016/j.cyto.2016.01.021 ... IL-1α and TNF are both acute-phase cytokines that act to promote fever and inflammation. There are, in fact, few examples in ...

https://en.wikipedia.org/wiki/Interleukin_1-alpha

Despite cytokines often being too large to pass through the blood-brain barrier alone, their effect on the central nervous ... One important inflammatory cytokine, interferon-α (IFN- α), is correlated with the development of depressive symptoms through ... Due to this sensitivity and NLPR3's role in triggering cytokine release, NLPR3 is thought to be a key component in sterile ... This is due to cytokines being directly involved with inflammatory responses while also serving as a signal that can lead to ...

https://en.wikipedia.org/wiki/Depression_and_immune_function

"Committees". Cytokines-interferons. Retrieved 17 October 2016. Parallelus (24 May 1990). "Bryan R.G. Williams, Ph.D. - The ... "Newsletter" (PDF). Cytokines-interferons.org. Archived from the original (PDF) on 16 October 2015. Retrieved 17 October 2016. " ... and was chair of the publications committee of the International Cytokine and Interferon Society from 2010 to 2016. 1990: ... President of the International Society for Interferon and Cytokine Research 2005: Maurice Saltzman Award, The Mt Sinai Health ...

https://en.wikipedia.org/wiki/Bryan_Williams_(professor)

IL-7 is a cytokine important for B and T cell development. This cytokine and the hepatocyte growth factor (HGF) form a ... This cytokine is found to be a cofactor for V(D)J rearrangement of the T cell receptor beta (TCRß) during early T cell ... This cytokine can be produced locally by intestinal epithelial and epithelial goblet cells, and may serve as a regulatory ... A study also demonstrate how the autocrine production of the IL-7 cytokine mediated by T-cell acute lymphoblastic leukemia (T- ...

https://en.wikipedia.org/wiki/Interleukin_7

IL7R-α is a type I cytokine receptor and is a subunit of the functional Interleukin-7 receptor and Thymic Stromal Lymphopoietin ... Appasamy PM (1999). "Biological and clinical implications of interleukin-7 and lymphopoiesis". Cytokines Cell. Mol. Ther. 5 (1 ... Type I cytokine receptors, Clusters of differentiation, All stub articles, Membrane protein stubs). ...

https://en.wikipedia.org/wiki/Interleukin-7_receptor-α

Stimulation of myeloblasts by G-CSF and other cytokines triggers maturation, differentiation, proliferation and cell survival. ... "Hematopoietic cytokines". Blood. 111 (2): 485-91. doi:10.1182/blood-2007-03-079681. PMC 2200848. PMID 18182579. Figure 12-14 in ...

https://en.wikipedia.org/wiki/Myeloblast

Kelso, Anne; Clouston, Andrew (1996), Cytokines in transplantation, R.G. Landes ; New York : Chapman & Hall, ISBN 978-3-540- ... particularly the cellular and molecular control of cytokine synthesis and cytolytic activity. As Director of the WHO ... 60731-1 Kelso, Anne; Clouston, Andrew (1996). Cytokines in transplantation. Austin : R.G. Landes ; New York : Chapman & Hall. ...

https://en.wikipedia.org/wiki/Anne_Kelso

The activated caspase-1 finally cleaves the immature pro-inflammatory cytokines pro-IL-1β and pro-IL-18, as well as Gasdermin-D ... Cayrol C, Girard JP (June 2009). "The IL-1-like cytokine IL-33 is inactivated after maturation by caspase-1". Proceedings of ... Caspase-1 activates maturation of proinflammatory cytokines (IL-1β, IL-18). Like AIM2, IFI16 (IFN-inducible protein 16) belongs ... The NLRP3 inflammasome can then mediate processing of pro-inflammatory cytokines and result in release of IL-1β and IL-18 in ...

https://en.wikipedia.org/wiki/Inflammasome

Cytokines & Inflammation (1). US application 2010305210, Barkan R, Ghicavii V, "S-Alkylisothiouronium Derivatives for Treating ...

https://en.wikipedia.org/wiki/S-Ethylisothiouronium_diethylphosphate

177-8. ISBN 978-0-19-858170-3. Tedgui, Alain; Mallat, Ziad (2006). "Cytokines in Atherosclerosis". Physiological Reviews. ...

https://en.wikipedia.org/wiki/1833_in_science

Baliwag J, Barnes DH, Johnston A (June 2015). "Cytokines in psoriasis". Cytokine. Skin Disease, Immune Response and Cytokines. ... Kunz M, Ibrahim SM (2009). "Cytokines and cytokine profiles in human autoimmune diseases and animal models of autoimmunity". ... can reduce the number of dendritic cells and favors a Th2 cell cytokine secretion pattern over a Th1/Th17 cell cytokine profile ... Other cytokines such as IL-17 and IL-22 also have been targets for inhibition as they play important roles in the pathogenesis ...

https://en.wikipedia.org/wiki/Psoriasis

Baliwag J, Barnes DH, Johnston A (June 2015). "Cytokines in psoriasis". Cytokine. 73 (2): 342-50. doi:10.1016/j.cyto.2014.12. ... IL-17 induces the production of many other cytokines (such as IL-6, G-CSF, GM-CSF, IL-1β, TGF-β, TNF-α), chemokines (including ... The release of cytokines causes many functions, such as airway remodeling, a characteristic of IL-17 responses. The increased ... The active form of vitamin D has been found to 'severely impair' production of the IL-17 and IL-17F cytokines by Th17 cells. ...

https://en.wikipedia.org/wiki/Interleukin_17

WHO Expert Committee on Biological Standardization (‎1999 : Geneva, Switzerland)‎; World Health Organization (‎World Health OrganizationWorld Health Organization, 2002)‎ ...

https://extranet.who.int/iris/restricted/browse?authority=Cytokines&type=mesh

http://www.copewithcytokines.de/cope.cgi?key=CD340

However, the in vivo cytokine cues and downstream pathways governing the differentiation of these cells are unclear. Here, we ... Cytokine-dependent induction of CD4+ T cells with cytotoxic potential during influenza virus infection J Virol. 2013 Nov;87(21 ... However, the in vivo cytokine cues and downstream pathways governing the differentiation of these cells are unclear. Here, we ...

https://pubmed.ncbi.nlm.nih.gov/23986597/

Cytokine storms cause the immune system to attack organs, such as the lungs, that they should be protecting. Can the drug ... These "cytokine storms" cause the immune system to attack organs, such as the lungs, that they should be protecting. ... patients at Robert Wood Johnson University Hospital in New Jersey to determine if it can regulate the onslaught of cytokine ... cases of acute respiratory distress and death in COVID-19 patients have been linked to an overactive response by cytokines, ...

https://www.futurity.org/covid-19-cytokine-storms-clinical-trial-edp1815-2358782/

When the production of these same cytokines is uncontrolled, immunologists describe the situation as a "cytokine storm." During ... Path to a cytokine storm. Heres how an overreaction from the immune system can endanger a person fighting off an infection. ... These cytokines can increase heartbeat, elevate body temperature, trigger blood clots that trap the pathogen and stimulate the ... Drugs that break the cytokine storm. One strategy behind the treatments for COVID is, in part, based in part on breaking the ...

https://theconversation.com/blocking-the-deadly-cytokine-storm-is-a-vital-weapon-for-treating-covid-19-137690

Abnormal Cytokine Levels in Idiopathic Dilated Cardiomyopathy Correlate with Prognosis JH Goldman; JH Goldman ... Abnormal Cytokine Levels in Idiopathic Dilated Cardiomyopathy Correlate with Prognosis. Clin Sci (Lond) 1 July 1995; 89 (s33): ...

https://portlandpress.com/clinsci/article-abstract/89/s33/4P/106982/Abnormal-Cytokine-Levels-in-Idiopathic-Dilated?redirectedFrom=fulltext

Huang W, Tang Y and Li L: HMGB1, a potent proinflammatory cytokine in sepsis. Cytokine. 51:119-126. 2010. View Article : Google ... Detection of inflammatory cytokine content by ELISA assay. All ELISA procedures strictly followed the protocols provided by the ... Inhibitory effects of miR‑25 targeting HMGB1 on macrophage secretion of inflammatory cytokines in sepsis. *Authors: *Chunyan ... Zhu C, Chen T and Liu B: Inhibitory effects of miR‑25 targeting HMGB1 on macrophage secretion of inflammatory cytokines in ...

https://www.spandidos-publications.com/10.3892/ol.2018.9308

... Pakistan Journal of Biological Sciences, 12: 1376-1380. DOI: 10.3923/pjbs. ... Since the immune response during human amoebiasis has not been clearly defined, we chose to evaluate cytokine production in ... Th-1/Th-2 Cytokine Pattern in Human Amoebic Colitis table, th, td { border: 0px solid #ececec; border-collapse: collapse; } th ...

https://scialert.net/abstract/?doi=pjbs.2009.1376.1380

B31 PNEUMONIA, ACUTE RESPIRATORY INFECTION: Acute Ethanol Treatment Inhibits Cytokine-Induced Nuclear Factor-Kb (nf-Kb) ...

https://www.proquest.com/openview/d890c2fc76d377cb9e6d7af16ec361aa/1?pq-origsite=gscholar&cbl=40575

Cytokines are protein mediators of intercellular stress communication with autocrine, paracrine, and endocrine modes of action ... IL-21 is a member of the class I cytokine receptor-binding cytokine family including leptin, IL-2-7, IL-9, IL-11-13, and IL-15 ... Cytokines and Type 1 Diabetes: A Numbers Game Lars Groth Grunnet; Lars Groth Grunnet ... A number of cytokines have been shown to be important for the development of type 1 diabetes both at the level of the immune ...

https://diabetesjournals.org/diabetes/article/60/3/697/33540/Cytokines-and-Type-1-Diabetes-A-Numbers-Game

Cytokine plasma levels were determined by ELISA. Possible associations between miR-155 levels and serum cytokine concentrations ... Thus, our results suggest that miR-155 might be involved in the pathogenesis of ITP by regulating cytokine profiles, which may ... suppressor of cytokine signaling) mRNA in peripheral blood mononuclear cells (PBMCs) from 28 ITP patients and 28 healthy ... Expression in Peripheral Blood Mononuclear Cells of Primary Immune Thrombocytopenia Patients Was Correlated with Serum Cytokine ...

https://karger.com/aha/article-abstract/133/3/257/15145/Increased-miR-155-Expression-in-Peripheral-Blood?redirectedFrom=fulltext

http://www.copewithcytokines.org/cope.cgi?key=LAMB3

Cytokines. en_US. dc.title. Role of the Cytokine of Macrophage Migration Inhibitory Factor (MIF) in Inner Ear Neuronal and ... Role of the Cytokine of Macrophage Migration Inhibitory Factor (MIF) in Inner Ear Neuronal and Sensory Cell Development.. dc. ... Cytokine arrays and proteomic studies demonstrated that the bioactive components of ODF include Macrophage Migration Inhibitory ...

https://deepblue.lib.umich.edu/handle/2027.42/78980?show=full

Suppressor of cytokine signalling 1 (SOCS1) is a physiological regulator of the asthma response.. Lee C, Kolesnik TB, Caminschi ... Suppressor of cytokine signalling 1 (SOCS1) is a negative regulator of IL-4-dependent pathways in vitro and might therefore ... Expression of the Th2 cytokines, IL-4, IL-5 and IL-13 was increased in CD4+ cells and lung tissue from OVA-treated Socs1(-/-) ... It is at present unclear whether the elevated cytokine levels are sufficient to result in the exacerbated Th2 response to OVA ...

https://www.burnet.edu.au/knowledge-and-media/research-articles/suppressor-of-cytokine-signalling-1-socs1-is-a-physiological-regulator-of-the-asthma-response/

Graphene-Based Materials for the Fast Removal of Cytokines from Blood Plasma. ... Graphene-Based Materials for the Fast Removal of Cytokines from Blood Plasma ... Graphene-Based Materials for the Fast Removal of Cytokines from Blood Plasma, ACS Applied Bio Materials, vol. 1, no. 2, 2018, ... Graphene-Based Materials for the Fast Removal of Cytokines from Blood Plasma}, journal = {ACS Applied Bio Materials}, volume ...

https://nano.materials.drexel.edu/wp-publications/571/

The cytokine-induced killer cells (CIK) have been reported to have potent cytotoxicity against a variety of tumor cells ... The cytokine-induced killer cells (CIK) have been reported to have potent cytotoxicity against a variety of tumor cells ... Role of NKG2D in cytokine-induced killer cells against multiple myeloma cells.. Feb 18, 2021 ...

https://www.physiciansweekly.com/301327/

COVID-19: consider cytokine storm syndromes and immunosuppression. Lancet 2020;395:1033-4.doi:10.1016/S0140-6736(20)30628-0 ... On the alert for cytokine storm: immunopathology in COVID-19. Arthritis Rheumatol 2020;72:1059-63.doi:10.1002/art.41285 pmid: ... Cytokine storm syndrome (CSS), a state of systemic hyperinflammation, is a rare and potentially lethal complication of various ... COVID-19-associated cytokine storm syndrome (CSS) is an important complication of severe acute respiratory syndrome coronavirus ...

https://ard.bmj.com/content/79/9/1143?ijkey=63f208b200e48121eb38408c0c34c7d9dd57af18&keytype2=tf_ipsecsha

Enhancement of chicken macrophage cytokine response to Salmonella Typhimurium when combined with bacteriophage P22. ... Also, four cytokine (IL-4, IL-8, IL-10, and IFN-γ) gene expression levels in the presence of LT2 and/or P22 were quantified by ... Enhancement of chicken macrophage cytokine response to Salmonella Typhimurium when combined with bacteriophage P22.. Title. ... The ELISA indicated that HD-11 cells produced significantly higher IL-8 cytokine levels in the supernatant during the ...

https://cropandsoil.oregonstate.edu/biblio/enhancement-chicken-macrophage-cytokine-response-salmonella-typhimurium-when-combined

The results of our study show that both the pro-inflammatory cytokine IFNγ and the potent anti-inflammatory cytokine IL-10 were ... secreting the cytokine interferon-gamma (IFNγ) that inhibits Th2 cell differentiation. Th2 cells produce cytokine interleukins ... our data suggest that the anti-inflammatory cytokine IL-10 and the pro-inflammatory cytokines IFNγ play important roles in the ... T-cell cytokine production and endothelial dysfunction in type 2 diabetic patients with nephropathy ...

https://www.emro.who.int/emhj-volume-15-2009/volume-15-issue-4/t-cell-cytokine-production-and-endothelial-dysfunction-in-type-2-diabetic-patients-with-nephropathy.html

This kit may be used for the analysis of the above cytokines and chemokines in rat serum, plasma, other rat biological fluids, ... SENSITIVITY: 1.31 - 54.42 pg/mL; Refer to kit protocol for sensitivities for individual cytokines/chemokines. ... manu factured by LINCO Research is to be used for the simultaneous quantification of the following twenty four rat cytokines/ ...

https://lincoresearch.com/products/rcyto-80k.html

The cytokine release symptoms (CRS), which includes been reported in severe COVID 19 cases, is the effect of a dysregulated web ... The cytokine release symptoms (CRS), which includes been reported in severe COVID 19 cases, is the effect of a dysregulated web ... It can nevertheless end up being deduced that therapies targeted at reducing the degrees of pro-inflammatory cytokines may be ... The cytokine discharge syndrome (CRS), Taranabant racemate which includes been MBP reported in serious COVID 19 situations, is ...

https://fabretp.org/2023/03/21/the-cytokine-release-symptoms-crs-which-includes-been-reported-in-severe-covid-19-cases-is-the-effect-of-a-dysregulated-web-host-immune-response-mediated-by-pro-inflammatory-cytokines-wit/

The ERS-education website provides centralised access to all educational material produced by the European Respiratory Society. It is the worlds largest CME collection for lung diseases and treatment offering high quality e-learning and teaching resources for respiratory specialists. This distance learning portal contains up-to-date study material for the state-of-the-art in Pulmonology.

https://dev.ers-education.org/lr/show-details/?idP=128976

... Poster Published ...

https://www.technologynetworks.com/diagnostics/posters/targeting-inflammatory-cytokines-using-adenoviruses-gene-delivery-of-biological-therapies-in-ovarian-cancer-230318

Bovine Cytokine Elisa. Lab Reagents Bovine Elisa Laboratories manufactures the bovine cytokine elisa reagents distributed by ... The Bovine Cytokine Elisa reagent is RUO (Research Use Only) to test human serum or cell culture lab samples. To purchase these ... Description: A polyclonal antibody raised in Rabbit that recognizes and binds to Human Cytokine IK . This antibody is tested ... Description: A sandwich ELISA for quantitative measurement of Goat Suppressors Of Cytokine Signaling 3 in samples from blood, ...

https://www.mugen-noe.org/bovine-cytokine-elisa/

Mechanism of suppressors of cytokine signaling 1 inhibition of epithelial-mesenchymal transition signaling through ROS ... Keywords: suppressors of cytokine signaling, reactive oxygen species, Src, thioredoxin, EMT signaling ... We have investigated the role of suppressors of cytokine signaling (SOCS)1 as an inhibitor of ROS-induced EMT using colon ...

https://www.oncotarget.com/article/11537/

These studies have indicated that most cytokines examined are expressed at the mRNA levels at least, and many other cytokines ... Other workers and ourselves have found that cell-cell contact is an important signal for the induction of cytokines, and our ... Several groups have documented the expression of cytokines in rheumatoid arthritis synovial tissue over the past 15 years or so ... Cytokine disequilibrium induced by cytokine-stimulated T cells (Tck). Mφ, monocytes; Ttcr, T-cell-receptor-dependent stimulated ...

https://arthritis-research.biomedcentral.com/articles/10.1186/ar556

A panel of 13 pro- and anti-inflammatory cytokines were quantified from serum in 175 participants [n = 84 Healthy Controls (HC ... Specifically, frontal thickness was positively associated with IFNγ, IL4, IL5 and IL13 cytokine levels in the healthy control ... Using moderation analysis, we then determined the extent to which individual variation in select cytokines, and their ... We found significant interactions between cytokine level and diagnosis on brain structure. Diagnostic status significantly ...

https://minerva-access.unimelb.edu.au/items/9029e977-93b0-522c-8d3d-8fe299c8783e

Click here to view all the Cytokines we offer you and your research. ... Give your research the best chance of success by using ProMabs Cytokines. ...

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Learn more about Cytokines & Growth Factors. We enable science by offering product choice, services, process excellence and our ...

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IL-21 is a member of the class I cytokine receptor-binding cytokine family including leptin, IL-2-7, IL-9, IL-11-13, and IL-15 ( 4 ) and signals via the JAK-STAT3 pathway to drive immunoglobulin production and proliferation of T- and B-cells as well as natural killer cells. (diabetesjournals.org)

Researchers will give the drug, EDP1815, developed by Evelo Biosciences Inc., to newly hospitalized COVID-19 patients at Robert Wood Johnson University Hospital in New Jersey to determine if it can regulate the onslaught of cytokine proteins-which cause the immune system to malfunction and become deadly-and is the reason for severe cases of respiratory distress and death. (futurity.org)
Many of the most severe cases of acute respiratory distress and death in COVID-19 patients have been linked to an overactive response by cytokines, proteins in the cells that signal a reaction by the immune system. (futurity.org)
White blood cells called macrophages use a set of sensors to recognize the pathogen and produce proteins called cytokines, which trigger inflammation and recruit other cells of the innate immune system for help. (theconversation.com)
Hormones differ from cytokines by being produced in specialized glandular organs, by not all being proteins, and by their homeostatic properties. (diabetesjournals.org)
These studies have indicated that most cytokines examined are expressed at the mRNA levels at least, and many other cytokines are found in abundance as proteins. (biomedcentral.com)
Cytokines are soluble proteins produced by one or more than cells. (bvsalud.org)

They do this by blocking the ability of macrophages to release cytokines and alert the rest of the immune system. (theconversation.com)
High mobility group box 1 (HMGB1) can promote the migration of macrophages and the release of inflammatory cytokines, functions associated with the occurrence of sepsis. (spandidos-publications.com)
HMGB1 serves a key role in the occurrence and progression of sepsis, and its production is induced by secretions of immune cells, including mononuclear cells, dendritic cells, macrophages stimulated by endotoxins, and inflammatory cytokines ( 2 ). (spandidos-publications.com)
A previous study demonstrated that HMGB1 could promote the migration of macrophages and the release of various inflammatory cytokines, causing aggregation of a variety of immune cells and inducing the inflammatory responses of sepsis ( 3 ). (spandidos-publications.com)
MWCNTs and C60F induced time-dependent polarization of M1 macrophages with a peak at day 1 and subsequently of M2 macrophages with a peak at day 7 in the lung, accompanied by elevated levels of type 1 or type 2 cytokines, respectively. (cdc.gov)

A new clinical trial is testing the safety and efficacy of an oral anti-inflammatory drug that could help prevent serious illness and death from "cytokine storms" in early-stage COVID-19 patients. (futurity.org)
The role of microRNA (miR)‑25 in the targeted regulation of HMGB1 expression and the release of macrophage inflammatory cytokines remains uncharacterized. (spandidos-publications.com)
Inhibiting expression of miR‑25 may serve a role in upregulating HMGB1 expression, promoting the secretion of inflammatory cytokines and resulting in sepsis. (spandidos-publications.com)
miRs are highly conserved, endogenous, non-coding small RNAs, which can regulate the expression of target genes by complete or incomplete complementary pairing with the 3′-untranslated region (3′-UTR) of the mRNA, serving an important role in immune cell activation, inflammatory cytokine release and the immune response ( 6 , 7 ). (spandidos-publications.com)
7 ) in 2009, who showed that β-cell overexpression of IL-21 caused inflammatory cytokine and chemokine induction, insulitis, β-cell destruction, and diabetes in nondiabetes-prone mice. (diabetesjournals.org)
ABSTRACT This study assessed changes in serum levels of cytokines IFNγ and IL-10 (biomarkers of inflammatory changes) and soluble biomarkers sICAM-1 and sE-selectin (biomarkers of endothelial dysfunction) in diabetic patients with and without nephropathy. (who.int)
It can nevertheless end up being deduced that therapies targeted at reducing the degrees of pro-inflammatory cytokines may be of great benefit to sufferers with serious COVID-19. (fabretp.org)
While such therapies targeting TNF in chronic inflammatory disease are very successful [ 2 ], it is also apparent that long-term blockade of a cytokine such as TNF, which is important in innate and acquired immunity, may lead to an increase in latent and/or opportunistic infections. (biomedcentral.com)
It has been observed that while the production of proinflammatory cytokines and enzymes is increased in RA, this is offset to some degree by the action of the endogenous anti-inflammatory cytokines and cytokine inhibitors. (biomedcentral.com)
This study assessed changes in serum levels of cytokines IFNgamma and IL-10 [‎biomarkers of inflammatory changes]‎ and soluble biomarkers sICAM-1 and sE-selectin [‎biomarkers of endothelial dysfunction]‎ in diabetic patients with and without nephropathy. (who.int)
Inflammasomes are key signaling platforms that detect microorganisms as well as sterile stressors, leading to the secretion of pro-inflammatory cytokines, e.g. (cdc.gov)

Cytokine Secretion Analyses. (cdc.gov)
We also performed cytokine profiling using a multiplex assay, and IL-1beta secretion was monitored using ELISA, in HMDMs primed or not with lipopolysaccharide (LPS). (cdc.gov)
This recognition process involves the generation and secretion of the cytokine, IFN-γ. (cdc.gov)

Concentrations of cytokines A) interleukin-8 (IL-8), B) interleukin-17A (IL-17A), C) granulocyte colony-stimulating factor (G-CSF), and D) granulocyte macrophage-colony-stimulating factor (GM-CSF) were measured in serum of patient 1 on days 0, 77, and 169 and in serum of patient 2 on days 0, 65, and 98. (cdc.gov)
The composition of infiltrating cells in the lung, serum IgE and IgG1 levels and cytokine levels were analysed. (edu.au)
This kit may be used for the analysis of the above cytokines and chemokines in rat serum, plasma, other rat biological fluids, tissue/ cell extracts, or cell culture supernatants. (lincoresearch.com)
The Bovine Cytokine Elisa reagent is RUO (Research Use Only) to test human serum or cell culture lab samples. (mugen-noe.org)
Description: Quantitativesandwich ELISA kit for measuring Human Cytokine-like protein 1 (CYTL1) in samples from serum, plasma, tissue homogenates. (mugen-noe.org)
Description: A sandwich ELISA for quantitative measurement of Goat Suppressors Of Cytokine Signaling 3 in samples from blood, plasma, serum, cell culture supernatant and other biological fluids. (mugen-noe.org)
Recently, we analyzed serum biomarkers by using samples from the Gulu outbreak and identified associations between cytokines/chemokines, acute-phase reactants, markers of coagulopathy, and markers of endothelial function and patient death, hemorrhage, and viremia. (cdc.gov)

Cytokine-like factor-1, a novel soluble protein, shares homology with members of the cytokine type I receptor family. (medlineplus.gov)

The cytokine group of molecules encompasses several hundred individual protein moieties, including 37 interleukins (ILs) and a multitude of chemokines. (diabetesjournals.org)
Refer to kit protocol for sensitivities for individual cytokines/chemokines. (lincoresearch.com)

The actual mechanism of β-cell destruction is still unclear, and classical T-cell effector pathways as well as many proinflammatory cytokines have been proven dispensable in transgenic animal models. (diabetesjournals.org)
It is now well accepted that the spontaneous production of proinflammatory cytokines (in particular, tumour necrosis factor [TNF] and IL-1) produced locally in the inflamed synovial joint contribute directly/indirectly to the pathogenesis of rheumatoid arthritis (RA) [ 1 ]. (biomedcentral.com)
There is thus a need to understand what mechanisms lead to the production of proinflammatory cytokines in RA synovial tissue, and further to determine how this is linked to homeostatic regulation. (biomedcentral.com)
There is therefore an important need to develop therapies that block proinflammatory pathways but leave unaffected those pathways that regulate immunoregulatory cytokines such as IL-10. (biomedcentral.com)

Role of the Cytokine of Macrophage Migration Inhibitory Factor (MIF) in Inner Ear Neuronal and Sensory Cell Development. (umich.edu)
Cytokine arrays and proteomic studies demonstrated that the bioactive components of ODF include Macrophage Migration Inhibitory Factor (MIF). (umich.edu)
Enhancement of chicken macrophage cytokine response to Salmonella Typhimurium when combined with bacteriophage P22. (oregonstate.edu)
Other workers and ourselves have found that cell-cell contact is an important signal for the induction of cytokines, and our work has demonstrated that tumour necrosis factor and IL-10 production in rheumatoid arthritis synovial joint cells cultures is dependent on T cell/macrophage interaction. (biomedcentral.com)

Cytokines are central mediators of inflammation by controling innate and adaptive immune responses as well as tissue damage, defense, repair, and remodeling. (diabetesjournals.org)
Suppressor of cytokine signalling 1 (SOCS1) is a negative regulator of IL-4-dependent pathways in vitro and might therefore control T-helper type 2 (Th2) immunity associated traits, such as IgE levels, mucin production, IL-5 and IL-13 induction, and eosinophilic mucosal inflammation, which are implicated in allergic asthma. (edu.au)
Oncostatin M (OSM), as a member of the Interleukin-6 family cytokines , plays a significant role in inflammation , autoimmunity , and cancers . (bvsalud.org)

The cytokine-induced killer cells (CIK) have been reported to have potent cytotoxicity against a variety of tumor cells including multiple myleoma (MM) cells. (physiciansweekly.com)

However, the in vivo cytokine cues and downstream pathways governing the differentiation of these cells are unclear. (nih.gov)

Cytokines essential for recruitment or maturation of neutrophils in 2 patients infected with Candidatus Neoehrlichia mikurensis, Sweden. (cdc.gov)
Others cytokines - such as interleukin 1b, interleukin 6 and tumor necrosis factor - guide neutrophils from the blood vessels to the infected tissue. (theconversation.com)

Cytokine levels below the 33 limit of detection were set to one-half the minimum detectable level for the assay. (cdc.gov)

The CRLF1 gene provides instructions for making a protein called cytokine receptor-like factor 1 (CRLF1). (medlineplus.gov)

It is debated whether cytokines also have homeostatic properties, i.e., contribute to the maintenance of normal cellular physiology. (diabetesjournals.org)

It is at present unclear whether the elevated cytokine levels are sufficient to result in the exacerbated Th2 response to OVA challenge or whether enhanced intra-cellular signalling also contributes. (edu.au)
Also, four cytokine (IL-4, IL-8, IL-10, and IFN-γ) gene expression levels in the presence of LT2 and/or P22 were quantified by qRT-PCR. (oregonstate.edu)
Studies using these samples found associations between fatal outcomes and elevated liver enzyme levels, renal dysfunction, cytokine dysregulation, and genetic factors. (cdc.gov)

Expression of the Th2 cytokines, IL-4, IL-5 and IL-13 was increased in CD4+ cells and lung tissue from OVA-treated Socs1(-/-)Ifngamma(-/-) mice. (edu.au)
Several groups have documented the expression of cytokines in rheumatoid arthritis synovial tissue over the past 15 years or so. (biomedcentral.com)
The main cytokines that are founded on the health periodontal tissue are: the fibroblast growth factor, the plated-derived growth factor, the insulin-like growth factor and growth factor. (bvsalud.org)

Bovine Elisa Laboratories manufactures the bovine cytokine elisa reagents distributed by Genprice. (mugen-noe.org)

Cytokines are protein mediators of intercellular stress communication with autocrine, paracrine, and endocrine modes of action. (diabetesjournals.org)
This protein partners with a similar protein called cardiotrophin-like cytokine factor 1 (CLCF1), which is produced from the CLCF1 gene. (medlineplus.gov)

Objectives To prospectively investigate in patients with severe COVID-19-associated cytokine storm syndrome (CSS) whether an intensive course of glucocorticoids with or without tocilizumab accelerates clinical improvement, reduces mortality and prevents invasive mechanical ventilation, in comparison with a historic control group of patients who received supportive care only. (bmj.com)

These cytokines can increase heartbeat, elevate body temperature, trigger blood clots that trap the pathogen and stimulate the neurons in the brain to modulate body temperature, fever, weight loss and other physiological responses that have evolved to kill the virus. (theconversation.com)

These "cytokine storms" cause the immune system to attack organs, such as the lungs, that they should be protecting. (futurity.org)
A number of cytokines have been shown to be important for the development of type 1 diabetes both at the level of the immune system and at the level of the target β-cells ( 2 , 3 ). (diabetesjournals.org)

26 in cytokine expression: C t (stimulated) - C t (unstimulated) = C t . (cdc.gov)

Virtually all nucleated cells produce and respond to cytokines under defined conditions, mainly in response to stress signals and in parallel to their differentiated functions. (diabetesjournals.org)
Role of NKG2D in cytokine-induced killer cells against multiple myeloma cells. (physiciansweekly.com)
Importantly, we observed that the manner in which T cells were activated influenced the profile of cytokines induced in the monocytes. (biomedcentral.com)
However, if the T cells were stimulated with a cocktail of cytokines (TNF-α, IL-2 and IL-6) for 8 days (bystander activation), TNF-α production followed but IL-10 production did not [ 11 ]. (biomedcentral.com)

We have investigated the role of suppressors of cytokine signaling (SOCS)1 as an inhibitor of ROS-induced EMT using colon cancer cell lines transduced with SOCS1 and shSOCS1. (oncotarget.com)

When the production of these same cytokines is uncontrolled, immunologists describe the situation as a "cytokine storm. (theconversation.com)
Since the immune response during human amoebiasis has not been clearly defined, we chose to evaluate cytokine production in patients suffering from amoebic colitis. (scialert.net)
Interestingly, T-cell numbers, regulatory T-cell activity and cytokine production were normal in these mice, suggesting that the effect was not a consequence of general immunosuppression as might be expected from the in vitro effects of IL-21 ( 4 ). (diabetesjournals.org)

Dotted lines indicate detection limit for each cytokine. (cdc.gov)

Suppressor of cytokine signalling 1 (SOCS1) is a physiological regulator of the asthma response. (edu.au)
1999. Response of normal human keratinocytes to sulfur mustard (HD): Cytokine release using a non-enzymatic detachment procedure. (cdc.gov)
2001). been shown to be one of the important causes of Cytokines are released in response to a diverse secondary immunodeficiency (Rosenblatt, 1996). (who.int)

RÉSUMÉ Cette étude a permis d'évaluer les modifications des taux sériques de cytokines IFNγ et IL-10 (biomarqueurs de modifications de l'état inflammatoire) et de biomarqueurs solubles sICAM-1 et sE-sélectine (biomarqueurs du dysfonctionnement endothélial) chez des patients diabétiques atteints et non atteints de néphropathie. (who.int)
Les IFNγ et les IL-10 étaient significativement élevés chez ceux qui présentaient une néphropathie diabétique (ND) et une maladie rénale en phase terminale (MRPT) par rapport aux témoins et aux patients diabétiques sans ND. (who.int)
Twenty five age-matched healthy acute leukaemia patients, cytokines could be subjects were taken as control group. (who.int)

During a cytokine storm, the blood vessels widen further (vasolidation), leading to low blood pressure and widespread blood vessel injury. (theconversation.com)
The cytokine storm is a centerpiece of the COVID-19 pathology with devastating consequences for the host. (theconversation.com)

Cytokines : basic principles and practical applications / editors, S. Romagnani and G. Del Prete, A. K. Abbas. (who.int)

Anatomy44

Organisms10

Diseases15

Chemicals and Drugs126

Analytical, Diagnostic and Therapeutic Techniques and Equipment22

Phenomena and Processes38

Disciplines and Occupations1

Information Science2

Health Care1

GM-CSF-deficient mice are susceptible to pulmonary group B streptococcal infection. (1/33104)

Socs1 binds to multiple signalling proteins and suppresses steel factor-dependent proliferation. (2/33104)

Interleukin-18 binding protein: a novel modulator of the Th1 cytokine response. (3/33104)

Differential regulation of vascular endothelial growth factor and its receptor fms-like-tyrosine kinase is mediated by nitric oxide in rat renal mesangial cells. (4/33104)

Borrelia burgdorferi spirochetes induce mast cell activation and cytokine release. (5/33104)

Potent immunoregulatory effects of Salmonella typhi flagella on antigenic stimulation of human peripheral blood mononuclear cells. (6/33104)

Clearance of Chlamydia trachomatis from the murine genital mucosa does not require perforin-mediated cytolysis or Fas-mediated apoptosis. (7/33104)

Effect of transforming growth factor beta on experimental Salmonella typhimurium infection in mice. (8/33104)

Cytokines

Tumor Necrosis Factor-alpha

Interleukin-6

Interleukin-1

Interferon-gamma

Cells, Cultured

Inflammation

Inflammation Mediators

Interleukin-10

Interleukin-4

Interleukin-1beta

Th2 Cells

Interleukins

Mice, Inbred C57BL

RNA, Messenger

Lipopolysaccharides

Interleukin-8

Chemokines

Th1 Cells

Signal Transduction

Macrophages

Mice, Inbred BALB C

Gene Expression Regulation

Mice, Knockout

Interleukin-12

NF-kappa B

Monocytes

Enzyme-Linked Immunosorbent Assay

Interleukin-13

T-Lymphocytes

Disease Models, Animal

Interleukin-2

Lymphocyte Activation

Granulocyte-Macrophage Colony-Stimulating Factor

Interleukin-17

Flow Cytometry

Dendritic Cells

Reverse Transcriptase Polymerase Chain Reaction

Cell Line

Up-Regulation

Leukocytes, Mononuclear

Immunity, Innate

Receptors, Cytokine

Gene Expression

CD4-Positive T-Lymphocytes

Interleukin-5

Cell Differentiation

Recombinant Proteins

Antigens, CD

Transforming Growth Factor beta

Interleukin-18

Lung

Chemokine CCL2

Spleen

Toll-Like Receptors

Interleukin 1 Receptor Antagonist Protein

Anti-Inflammatory Agents

Th17 Cells

Cytokine Receptor gp130

Membrane Glycoproteins

Macrophage Activation

Time Factors

Toll-Like Receptor 4

Coculture Techniques

Apoptosis

Interleukin-1alpha

Receptors, Interleukin

Biological Markers

Mice, Transgenic

Neutrophils

Oncostatin M

Immunologic Factors

Interleukin-11

Down-Regulation

Nitric Oxide Synthase Type II

Adjuvants, Immunologic

T-Lymphocyte Subsets

Macrophages, Peritoneal

Receptors, Interleukin-1

Th1-Th2 Balance