Chemokine CCL27
Chemokine CCL21
Chemokine CCL22
Chemokine CCL17
Chemokine CCL2
Chemokine CCL19
Chemokine CCL5
Chemokine CCL20
Chemokine CCL1
Chemokines, CC
Receptors, Chemokine
Chemokine CCL3
Chemokine CCL7
Chemokines
Receptors, CCR10
Chemokine CCL4
Chemokine CXCL12
Receptors, CCR1
Chemokine CXCL10
Chemokine CCL8
Receptors, CCR2
Chemokine CCL11
Chemokine CCL24
Receptors, CCR7
Receptors, CCR8
Chemokine CXCL1
Chemotaxis, Leukocyte
Receptors, CCR4
Chemokines, CXC
Chemokine CX3CL1
Macrophage Inflammatory Proteins
Receptors, CCR5
Receptors, CCR3
Cell Movement
Chemokine CXCL2
Chemokine CXCL13
Receptors, CXCR4
Chemokine CXCL11
Chemotaxis
Chemokine CXCL6
Cells, Cultured
Dendritic Cells
Chemokine CXCL5
Cytokines
Mice, Knockout
Receptors, CXCR3
Monocytes
Macrophages
Gene Expression Regulation
RNA, Messenger
T-Lymphocytes
Inflammation
Reverse Transcriptase Polymerase Chain Reaction
Enzyme-Linked Immunosorbent Assay
Flow Cytometry
Receptors, Interleukin-8B
Signal Transduction
Dermatitis, Atopic
Up-Regulation
Monocyte Chemoattractant Proteins
Disease Models, Animal
Skin
Mice, Transgenic
Interleukin-8
Ligands
Receptors, CCR6
CD4-Positive T-Lymphocytes
Receptors, Interleukin-8A
Lymph Nodes
NF-kappa B
Carbon Tetrachloride
Immunohistochemistry
Receptors, Cytokine
T-Lymphocytes, Regulatory
Tumor Necrosis Factor-alpha
Chemokines, CX3C
Receptors, CXCR5
Protein Binding
Chemotactic Factors
CD8-Positive T-Lymphocytes
Endothelial Cells
Lymphocyte Activation
Monokines
Receptors, HIV
Duffy Blood-Group System
Chemotactic Factors, Eosinophil
Neutrophil Infiltration
Neutrophils
Heterocyclic Compounds
Lung
Leukocytes
Gene Expression
Inflammation Mediators
Interferon-gamma
Th2 Cells
Cell Migration Inhibition
HIV-1
Molecular Sequence Data
Eosinophils
Intercellular Signaling Peptides and Proteins
Lipopolysaccharides
Down-Regulation
Amino Acid Sequence
Epithelial Cells
Leukocytes, Mononuclear
Th1 Cells
Lymphoid Tissue
T-Lymphocyte Subsets
Gene Expression Profiling
Platelet Factor 4
Stromal Cells
Immunity, Innate
Bronchoalveolar Lavage Fluid
Transfection
Drug-Induced Liver Injury
Endothelium, Lymphatic
Anti-monocyte chemoattractant protein-1/monocyte chemotactic and activating factor antibody inhibits neointimal hyperplasia in injured rat carotid arteries. (1/4001)
Monocyte chemoattractant protein-1 (MCP-1)/monocyte chemotactic and activating factor (MCAF) has been suggested to promote atherogenesis. The effects of in vivo neutralization of MCP-1 in a rat model were examined in an effort to clarify the role of MCP-1 in the development of neointimal hyperplasia. Competitive polymerase chain reaction analysis revealed maximum MCP-1 mRNA expression at 4 hours after carotid arterial injury. Increased immunoreactivities of MCP-1 were also detected at 2 and 8 hours after injury. Either anti-MCP-1 antibody or nonimmunized goat IgG (10 mg/kg) was then administered every 12 hours to rats that had undergone carotid arterial injury. Treatment with 3 consecutive doses of anti-MCP-1 antibody within 24 hours (experiment 1) and every 12 hours for 5 days (experiment 2) significantly inhibited neointimal hyperplasia at day 14, resulting in a 27.8% reduction of the mean intima/media ratio (P<0.05) in experiment 1 and a 43.6% reduction (P<0.01) in experiment 2. This effect was still apparent at day 56 (55.6% inhibition; P<0.05). The number of vascular smooth muscle cells in the neointima at day 4 was significantly reduced by anti-MCP-1 treatment, demonstrating the important role of MCP-1 in early neointimal lesion formation. However, recombinant MCP-1 did not stimulate chemotaxis of vascular smooth muscle cells in an in vitro migration assay. These results suggest that MCP-1 promotes neointimal hyperplasia in early neointimal lesion formation and that neutralization of MCP-1 before, and immediately after, arterial injury may be effective in preventing restenosis after angioplasty. Further studies are needed to clarify the mechanism underlying the promotion of neointimal hyperplasia by MCP-1. (+info)Infection of human endothelial cells with Chlamydia pneumoniae stimulates transendothelial migration of neutrophils and monocytes. (2/4001)
We have previously shown that different isolates of Chlamydia pneumoniae display heterogeneity in the in vitro stimulation of chemokines and adhesion molecules from infected human endothelial cells. In the present study, we examined the ability of different isolates of C. pneumoniae to promote transendothelial migration of neutrophils and monocytes. Human umbilical vein endothelial cells (HUVEC) were infected with low (<15)-passage C. pneumoniae isolates A-03, PS-32, and BR-393 and high (>40)-passage isolates BAL-16, TW-183, and T-2634, and levels of neutrophil and monocyte transendothelial migration were determined following 24 h of infection. Compared to mock-infected controls, significant increases in neutrophil migration were observed in response to most C. pneumoniae isolates examined (P < 0.001). Levels of monocyte migration were significantly increased in response to TW-183 and T-2634 (P < 0.001). Serial passage (>40 times) of the three low-passage isolates in HEp-2 cell cultures prior to infection of HUVEC generally resulted in the promotion of higher levels of neutrophil and monocyte transendothelial migration. These findings were compatible with differences observed in the extent of interleukin-8 (IL-8) and monocyte chemotactic protein-1 (MCP-1) stimulation between low- and high-passage A-03, PS-32, and BR-393. As opposed to C. pneumoniae, infection with C. trachomatis L2 caused only a slight increase in neutrophil transendothelial migration, which correlated with the lack of measurable IL-8 levels by this species. However, significant levels of monocyte migration were induced in response to C. trachomatis L2 despite a lack of measurable MCP-1 stimulation. C. trachomatis serovars A and E also failed to induce IL-8 and MCP-1 production in HUVEC. Results from this study indicate that the passage history of C. pneumoniae may play a role in the divergence of stimulatory activities observed among isolates in human endothelial cells. In addition, the differences observed between this organism and C. trachomatis suggest that the upregulation of IL-8 and MCP-1 in endothelial cells may be unique to C. pneumoniae. (+info)Luteal regression in the normally cycling rat: apoptosis, monocyte chemoattractant protein-1, and inflammatory cell involvement. (3/4001)
In hypophysectomized rats, prolactin induces regression of the corpora lutea. Luteal regression is accompanied by infiltration of monocytes/macrophages, declines in luteal mass and plasma progestins, and increased staining for monocyte chemoattractant protein-1 (MCP-1). We investigated whether similar events are induced during the estrous cycle, after the proestrous prolactin surge. Rats were killed on proestrus or on estrus, and one ovary was frozen for immunohistochemical detection of MCP-1, monocytes/macrophages (ED1-positive), and differentiated macrophages (ED2-positive) and for in situ detection of apoptotic nuclei. Corpora lutea of the current (proestrus) or preceding (estrus) cycle were dissected from the ovaries of additional rats and frozen for the same analyses and for determination of total protein content. In sections of whole ovaries, intensity and distribution of MCP-1 staining were increased in corpora lutea of multiple ages on estrus as compared to proestrus, as were numbers of differentiated macrophages and apoptotic nuclei per high-power field. Sections of isolated corpora lutea showed these increases on estrus, and the number of monocytes/macrophages per high-power field was also significantly increased. Accompanying these inflammatory/immune events, the corpora lutea on estrus showed decreased weight and total protein per corpus luteum, as compared to corpora lutea on proestrus. These changes are consistent with a proposed role for prolactin in the initiation of luteal apoptosis and of a sequence of inflammatory/immune events that accompany regression of the rat corpus luteum during the normal estrous cycle. (+info)Induction of macrophage C-C chemokine expression by titanium alloy and bone cement particles. (4/4001)
Particulate wear debris is associated with periprosthetic inflammation and loosening in total joint arthroplasty. We tested the effects of titanium alloy (Ti-alloy) and PMMA particles on monocyte/macrophage expression of the C-C chemokines, monocyte chemoattractant protein-1 (MCP-1), monocyte inflammatory protein-1 alpha (MIP-1alpha), and regulated upon activation normal T expressed and secreted protein (RANTES). Periprosthetic granulomatous tissue was analysed for expression of macrophage chemokines by immunohistochemistry. Chemokine expression in human monocytes/macrophages exposed to Ti-alloy and PMMA particles in vitro was determined by RT-PCR, ELISA and monocyte migration. We observed MCP-1 and MIP-1alpha expression in all tissue samples from failed arthroplasties. Ti-alloy and PMMA particles increased expression of MCP-1 and MIP-1alpha in macrophages in vitro in a dose- and time-dependent manner whereas RANTES was not detected. mRNA signal levels for MCP-1 and MIP-1alpha were also observed in cells after exposure to particles. Monocyte migration was stimulated by culture medium collected from macrophages exposed to Ti-alloy and PMMA particles. Antibodies to MCP-1 and MIP-1alpha inhibited chemotactic activity of the culture medium samples. Release of C-C chemokines by macrophages in response to wear particles may contribute to chronic inflammation at the bone-implant interface in total joint arthroplasty. (+info)Human immunodeficiency virus replication induces monocyte chemotactic protein-1 in human macrophages and U937 promonocytic cells. (5/4001)
We have recently described a significant correlation between human immunodeficiency virus-1 (HIV-1) RNA replication and monocyte chemotactic protein-1 (MCP-1) levels in the cerebrospinal fluid (CSF) of individuals with the acquired immunodeficiency syndrome (AIDS) with HIV encephalitis (E). Because local macrophages (microglia) are the cells predominantly infected in the brain, we investigated whether in vitro HIV infection affects MCP-1 production in mononuclear phagocytes (MP). MCP-1 secretion and expression were consinstently upregulated over constitutive levels in human monocyte-derived macrophages (MDM) infected with the M-tropic R5 BaL strain of HIV-1. HIV replication was required for this effect, as demonstrated by the absence of chemokine upregulation after infection in the presence of 3'-azido-3'-deoxythimidine (AZT) or cell-exposure to heat-inactivated (triangle up degrees ) virus. MCP-1 induction was not restricted to HIV-1 BaL, but was also observed during productive infection of MDM with two primary isolates differing for entry coreceptor usage and of U937 cells with the X4 HIV-1 MN strain. Based on the observation that exogenous HIV-1 Tat induced MCP-1 expression in astrocytes, we also investigated its role in MDM and U937 cells. Exogenous Tat induced MCP-1 production from MDM in a concentration-dependent manner, however, it was not effective on uninfected U937 cells or on the chronically infected U937-derived cell line U1. Transfection of Tat-expressing plasmids moderately activated HIV expression in U1 cells, but failed to induce MCP-1 expression in this cell line or in uninfected U937 cells. HIV replication-dependent expression of MCP-1 in MP may be of particular relevance for the pathogenesis of HIV infection in nonlymphoid organs such as the brain. (+info)Chemokine expression in CF epithelia: implications for the role of CFTR in RANTES expression. (6/4001)
To delineate the mechanisms that facilitate leukocyte migration into the cystic fibrosis (CF) lung, expression of chemokines, including interleukin-8 (IL-8), monocyte chemoattractant protein-1 (MCP-1), and RANTES, was compared between CF and non-CF airway epithelia. The findings presented herein demonstrate that, under either basal conditions or tumor necrosis factor-alpha (TNF-alpha)- and/or interferon-gamma (IFN-gamma)-stimulated conditions, a consistent pattern of differences in the secretion of IL-8 and MCP-1 between CF and non-CF epithelial cells was not observed. In contrast, CF epithelial cells expressed no detectable RANTES protein or mRNA under basal conditions or when stimulated with TNF-alpha and/or IFN-gamma (P +info)Angiotensin II plays a pathogenic role in immune-mediated renal injury in mice. (7/4001)
Several lines of evidence show the importance of angiotensin II (AII) in renal injuries, especially when hemodynamic abnormalities are involved. To elucidate the role of AII in immune-mediated renal injury, we studied anti-glomerular basement membrane (GBM) nephritis in AII type 1a receptor (AT1a)-deficient homozygous (AT1a-/-) and wild-type (AT1a+/+) mice. A transient activation of the renin-angiotensin system (RAS) was observed in both groups of mice at around day 1. A renal expression of monocyte chemoattractant protein-1 (MCP-1) was transiently induced at six hours in both groups, which was then downregulated at day 1. In the AT1a+/+ mice, after RAS activation, the glomerular expression of MCP-1 was exacerbated at days 7 and 14. Thereafter, severe proteinuria developed, and the renal expressions of transforming growth factor-beta1 (TGF-beta1) and collagen type I increased, resulting in severe glomerulosclerosis and interstitial fibrosis. In contrast, glomerular expression of MCP-1, proteinuria, and tissue damage were markedly ameliorated in the AT1a-/- mice. Because this amelioration is likely due to the lack of AT1a, we can conclude that AII action, mediated by AT1a, plays a pathogenic role in anti-GBM nephritis, in which AII may contribute to the exacerbation of glomerular MCP-1 expression. These results suggest the involvement of AII in immune-mediated renal injuries. (+info)MCP-1 deficiency reduces susceptibility to atherosclerosis in mice that overexpress human apolipoprotein B. (8/4001)
The earliest recognizable atherosclerotic lesions are fatty streaks composed of lipid-laden macrophages (foam cells). Circulating monocytes are the precursors of these foam cells, but the molecular mechanisms that govern macrophage trafficking through the vessel wall are poorly understood. Monocyte chemoattractant protein-1 (MCP-1), a member of the chemokine (chemotactic cytokine) family, is a potent monocyte agonist that is upregulated by oxidized lipids. Recent studies in hypercholesterolemic mice lacking apo E or the low-density lipoprotein receptor have suggested a role for MCP-1 in monocyte recruitment to early atherosclerotic lesions. To determine if MCP-1 is critically involved in atherogenesis in the setting of elevated physiological plasma cholesterol levels, we deleted the MCP-1 gene in transgenic mice expressing human apo B. Here we report that the absence of MCP-1 provides dramatic protection from macrophage recruitment and atherosclerotic lesion formation in apo B transgenic mice, without altering lipoprotein metabolism. Taken together with the results of earlier studies, these data provide compelling evidence that MCP-1 plays a critical role in the initiation of atherosclerosis. (+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.
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.
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.
The symptoms of carbon tetrachloride poisoning can vary depending on the level and duration of exposure, but may include:
* Respiratory problems, such as coughing, wheezing, and shortness of breath
* Nausea and vomiting
* Abdominal pain and diarrhea
* Headaches and dizziness
* Confusion and disorientation
* Slurred speech and loss of coordination
* Seizures and coma
If you suspect that you or someone else has been exposed to carbon tetrachloride, it is essential to seek medical attention immediately. Treatment for carbon tetrachloride poisoning typically involves supportive care, such as oxygen therapy and hydration, as well as medications to manage symptoms and remove the toxin from the body. In severe cases, hospitalization may be necessary.
Prevention is key when it comes to carbon tetrachloride poisoning. If you work with or are exposed to CTC, it is important to take safety precautions such as wearing protective clothing and equipment, using proper ventilation, and following all safety protocols. It is also essential to handle the chemical with care and store it in a safe location.
In conclusion, carbon tetrachloride poisoning can be a serious and potentially deadly condition that requires immediate medical attention. If you suspect exposure to CTC, it is crucial to seek medical help right away. By taking safety precautions and being aware of the risks associated with this chemical, you can prevent carbon tetrachloride poisoning and protect your health.
The definition of DILI has been revised several times over the years, but the most recent definition was published in 2013 by the International Consortium for DILI Research (ICDCR). According to this definition, DILI is defined as:
"A clinically significant alteration in liver function that is caused by a medication or other exogenous substance, and is not related to underlying liver disease. The alteration may be biochemical, morphological, or both, and may be acute or chronic."
The ICDCR definition includes several key features of DILI, including:
1. Clinically significant alteration in liver function: This means that the liver damage must be severe enough to cause symptoms or signs of liver dysfunction, such as jaundice, nausea, vomiting, or abdominal pain.
2. Caused by a medication or other exogenous substance: DILI is triggered by exposure to certain drugs or substances that are not related to underlying liver disease.
3. Not related to underlying liver disease: This means that the liver damage must not be caused by an underlying condition such as hepatitis B or C, alcoholic liver disease, or other genetic or metabolic disorders.
4. May be acute or chronic: DILI can occur as a sudden and severe injury (acute DILI) or as a slower and more insidious process (chronic DILI).
The ICDCR definition provides a standardized way of defining and diagnosing DILI, which is important for clinicians and researchers to better understand the cause of liver damage in patients who are taking medications. It also helps to identify the drugs or substances that are most likely to cause liver injury and to develop strategies for preventing or treating DILI.
CCL2
Chemokine
Monoclonal antibody therapy
Cytokine-like protein 1
5-Oxo-eicosatetraenoic acid
CC chemokine receptors
L-Ribonucleic acid aptamer
John S. K. Kauwe III
CCL7
CCR2
NR58-3.14.3
Adult neurogenesis
Specialized pro-resolving mediators
Monocyte
Carlumab
Noxxon Pharma
ML2-SA1
Coagulation factor II receptor
Broad-spectrum chemokine inhibitor
CGAS-STING cytosolic DNA sensing pathway
ARHGDIB
Interstitial nephritis
CCR4
Resistin
Major histocompatibility complex, class I-related
Index of immunology articles
Tumor microenvironment
Nivalenol
CCL8
CCL1
Dermal macrophage
MS100a7a15
Senescence-associated secretory phenotype
Leukocyte extravasation
Stimulator of interferon genes
Chromosome 17
Duffy antigen system
Immunologic Constant of Rejection
Keratinocyte
IL17A
Autoantibodies as Diagnostic Markers and Mediator of Joint Inflammation in Arthritis
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Publications 2016 | FAMRI
Pesquisa | Portal Regional da BVS
Amyloid-beta deposits lead to retinal degeneration in a mouse model of Alzheimer disease. - STOMICS DataBase
Unveiling the mysteries of salmonella typhi: the bacterium behind typhoid fever
Ligand2
- By in vitro and in vivo migration assays, we show that although CST itself is weakly chemotactic, it blocks migration of monocytes and granulocytes to inflammatory attracting factor CC-chemokine ligand 2 (CCL2) and macrophage inflammatory protein 2 (MIP-2). (biorxiv.org)
- We reported an association between intrathecal upregulation of C-C chemokine ligand 2(CCL2) and disease severity in ALS. (kyushu-u.ac.jp)
Cytokine2
- Results revealed no significant increase of proinflammatory cytokine/chemokine expressions. (cdc.gov)
- We analyze the effect of aging on gene expression and chemokine and cytokine networks and show an overall decreased expression of inflammatory mediators together with an increased expression of senescent cells recognition receptors. (elifesciences.org)
CXCL21
- and notably high expression of a set of chemokines that would favour neutrophil and monocyte recruitment including CXCL2, CCL2, CXCL12, CXCL1, CXCL6, CCL28. (garvan.org.au)
Cytokines and chemokines2
- Human Qbeads Inflammation Panel Kit allows the measurement of seven human cytokines and chemokines from either serum or in vitro samples. (sartorius.com)
- The integration of pathogen-associated molecular patterns (PAMPs) from microorganisms with their surface receptors in the immune cells, induces the production of several cytokines and chemokines that presents either a pro- and/or anti-inflammatory role by stimulating the secretion of a great variety of antibody subtypes and the activation of mechanisms of controlling the disease, such as the regulatory T cells. (bvsalud.org)
CCR21
- Ryo Yamasaki, Wataru Shiraishi, Yu Hashimoto, Senri Kou, Noriko Isobe, C-C chemokine receptor 2+ macrophages in nerves ameliorate motor neuron disease model mice, 63rd Annual meeting of the Japanese Society of Neurology, 2022.04, [Objective]Macrophages expressing C-C chemokine receptor type (2 CCR2)infiltrate into the neural tissues of amyotrophic lateral sclerosis(ALS)patients. (kyushu-u.ac.jp)
Inflammatory chemokines2
- Here, we report that CST blocks leukocyte migration towards inflammatory chemokines. (biorxiv.org)
- To compare the temporal and spatial expression patterns of amyloid precursor protein (APP), amyloid-beta deposits, inflammatory chemokines, and apoptosis in the retina of a mouse model of Alzheimer disease (AD). (cngb.org)
MCP12
CCL31
- Analytes offered in the Human Qbeads Inflammation Panel Kit include: Human Interferon gamma (IFNγ), Interleukin-2 (IL-2), Interleukin-6 (IL-6), CCL2 (MCP-1), CCL3 (MIP-1α), CXCL9 (MIG), and CXCL10 (IP-10). (sartorius.com)
MRNA1
- The mRNA levels of CCL2, C1ra, C1s, IL-18, IL-1β, TNFα, IL-33 and glial fibrillary acidic protein (GFAP) were significantly increased at day 1 post-RD, reduced gradually and, with the exception of GFAP and C1ra, returned to the basal levels by day 28 in WT mice. (biomedcentral.com)
Macrophage1
- Further, PACE ® treatment significantly decreased neutrophil and macrophage (white blood cell) infiltration into the wound, attenuating both CC- and CXC-chemokines at the wound margin. (sanuwave.com)
Macrophages1
- Surprisingly, Müller cells from IL-33 −/− mice expressed significantly lower levels of CCL2 and IL-6 compared with those from WT mice, particularly under hypoxic conditions, whereas IL-33 −/− bone marrow-derived macrophages expressed higher levels of inducible nitric oxide synthase, TNFα, IL-1β and CCL2 after LPS + IFNγ stimulation compared to WT macrophages. (biomedcentral.com)
Serum1
- Serum levels of CCL2 peaked twice during the immune response, once during the early, acute phase and again during the late, chronic phase. (elsevier.com)
Mediators1
- Interplay between several molecules (cytokines, chemokines, proteases, and inflammatory mediators) culminates in causing damage to the articular cartilage and bones. (hindawi.com)
Gene expression1
- 2016. Voluntary exercise blocks Western diet-induced gene expression of the chemokines CXCL10 and CCL2 in the prefrontal cortex. (uc.edu)
CXCL91
- In CSF, in patients without central nervous system (CNS) disease/infection, cytokines/chemokines are either undetectable (e.g., interleukin-6 [IL-6], CXCL8/IL-8, CXCL10/IP-10, CXCL9/MIG) or present at low levels (e.g. (cdc.gov)
Immune1
- To further elucidate the role of this chemokine in the anti-filarial immune response, we compared CCL2 deficient (CCL2 -/- ) mice to wild-type mice. (elsevier.com)
Migration1
- Barzilai S, Blecher-Gonen R, Barnett-Itzhaki Z, Zauberman A, Lebel-Haziv Y, Amit I, Alon R. M-sec regulates polarized secretion of inflammatory endothelial chemokines and facilitates CCL2-mediated lymphocyte transendothelial migration. (famri.org)
Mice2
- In IL-33 −/− mice, RD induced an exacerbated inflammatory response with significantly higher levels of CCL2, IL-1β and GFAP when compared to WT. (biomedcentral.com)
- We observed that CCL2 was expressed by peritoneal exudate cells and was present in the sera of wild-type mice. (elsevier.com)
Disease1
- The cytokines/chemokines included are implicated in inflammatory responses to disease states including autoimmune diseases, chronic inflammation, and infections, including viral infections such as COVID-19. (sartorius.com)
Human1
- These NF- kappaB activated islets not only expressed the same chemokine profile observed in human islets, but also struggled to maintain normoglycemia post transplantation. (garvan.org.au)
Patients2
Monocyte1
- Another reported that IL-10, C-X-C motif chemokine ligand 10 (CXCL-10, formerly IFN-γ inducible protein 10) and CC chemokine ligand 2 (CCL2, formerly monocyte chemoattractant protein 1) levels were higher in patients with high viral loads ( 12 ), but patients with severe disease had higher levels of CXCL10 and CCL2 than did patients with less-severe cases. (cdc.gov)
Epithelial Cells3
- This proposal will test the novel hypothesis that when L. reuteri are decreased due to stressor exposure, colonic epithelial cells overproduce chemokines (particularly CCL2) that increase the recruitment of inflammatory macrophages to the colon where they ultimately exacerbate colitis. (nih.gov)
- The first aim will examine the role of CCL2 as a novel primary mechanism (pathway) mediating the effects of stress on colonic inflammation, by assessing the effects of stress-induced alterations of L. reuteri on CCL2 production by colonic epithelial cells and by using CCL2 knockout mice. (nih.gov)
- Finally, in the third aim, we will determine whether the ability of L. reuteri to affect chemokine production by colonic epithelial cells is dependent upon L. reuteri colonizing the colon, and/or due to the production of immunomodulatory factor(s). (nih.gov)
Cytokines3
- Interferon pathway-related cytokines/chemokines, including interleukin (IL) 18, macrophage inflammatory protein 3α, and IL-33, were elevated, but tumor necrosis factor-α, IL-6, CXCL8 (formerly IL-8), and cytokines acting through C-C chemokine receptor 2 and CCR5 were lower among case-patients than controls. (cdc.gov)
- In addition to their primary role in mediating neuroinflammation, neuroimmune factors, such as cytokines, chemokines, and MHC, are essential for a variety of normal brain functions. (nih.gov)
- CCL2), cytokines (e.g. (nih.gov)
Receptors2
- The discussed chemokines in this review, their synonyms, receptors, activities and sources were summarized in Table 4 . (medscape.com)
- CCL3 in Cancers Chemokine receptors are expressed on APCs and are promising targets for idiotype (Id) vaccines, the V antigenic determinants region produced by B lymphomas and multiple myelomas. (medscape.com)
Proteins1
- Chemokines are a superfamily of secreted proteins involved in immunoregulatory and inflammatory processes. (nih.gov)
Role3
- In next part of the review, various chemokines with their specific role in altering immune response to combat various diseases especially cancers will be discussed. (medscape.com)
- [ 116 ] The role of CCL2 in tumor-development and progression is controversial. (medscape.com)
- C(C)Learing the Role of Chemokines in Pulmonary Fibrosis. (nih.gov)
Inflammation2
- Thus, modulation of EAE with C-C chemokine DNA vaccines is determined by targeting chemokines that are highly transcribed at the site of inflammation at the onset of disease. (medscape.com)
- LIF, CCL2 and IL-1alpha and the brain inflammation. (cdc.gov)
Activation1
- A chemokine that is a chemoattractant for MONOCYTES and may also cause cellular activation of specific functions related to host defense. (nih.gov)
Significant increase2
- Results revealed no significant increase of proinflammatory cytokine/chemokine expressions. (cdc.gov)
- Upon oral challenge with the murine colonic pathogen Citrobacter rodentium, which induces colonic histopathology with similarities to human IBD, mice exposed to SDR (and thus having lower levels of L. reuteri) had a significant increase in pathogen-induced colitis as indicated by a significant increase in colonic histopathology, chemokines (e.g. (nih.gov)
Studies1
- By contrast to above studies, expression of exogenous CCL2 by adenocarcinoma cells augmented the metastatic potential by modulating tumor-associated angiogenesis. (medscape.com)
Time1
- We examined cytokine/chemokine profiles of 9/12 case-patients compared with healthy controls at 3 time intervals. (cdc.gov)