ZymosanOpsonin Proteins: Proteins that bind to particles and cells to increase susceptibility to PHAGOCYTOSIS, especially ANTIBODIES bound to EPITOPES that attach to FC RECEPTORS. COMPLEMENT C3B may also participate.Phagocytosis: The engulfing and degradation of microorganisms; other cells that are dead, dying, or pathogenic; and foreign particles by phagocytic cells (PHAGOCYTES).Neutrophils: 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.Luminescent Measurements: Techniques used for determining the values of photometric parameters of light resulting from LUMINESCENCE.Macrophages: 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.)Superoxides: Highly reactive compounds produced when oxygen is reduced by a single electron. In biological systems, they may be generated during the normal catalytic function of a number of enzymes and during the oxidation of hemoglobin to METHEMOGLOBIN. In living organisms, SUPEROXIDE DISMUTASE protects the cell from the deleterious effects of superoxides.Latex: A milky, product excreted from the latex canals of a variety of plant species that contain cauotchouc. Latex is composed of 25-35% caoutchouc, 60-75% water, 2% protein, 2% resin, 1.5% sugar & 1% ash. RUBBER is made by the removal of water from latex.(From Concise Encyclopedia Biochemistry and Molecular Biology, 3rd ed). Hevein proteins are responsible for LATEX HYPERSENSITIVITY. Latexes are used as inert vehicles to carry antibodies or antigens in LATEX FIXATION TESTS.Leukotriene B4: The major metabolite in neutrophil polymorphonuclear leukocytes. It stimulates polymorphonuclear cell function (degranulation, formation of oxygen-centered free radicals, arachidonic acid release, and metabolism). (From Dictionary of Prostaglandins and Related Compounds, 1990)N-Formylmethionine Leucyl-Phenylalanine: A formylated tripeptide originally isolated from bacterial filtrates that is positively chemotactic to polymorphonuclear leucocytes, and causes them to release lysosomal enzymes and become metabolically activated.Luminol: 5-Amino-2,3-dihydro-1,4-phthalazinedione. Substance that emits light on oxidation. It is used in chemical determinations.Mannans: Polysaccharides consisting of mannose units.SRS-A: A group of LEUKOTRIENES; (LTC4; LTD4; and LTE4) that is the major mediator of BRONCHOCONSTRICTION; HYPERSENSITIVITY; and other allergic reactions. Earlier studies described a "slow-reacting substance of ANAPHYLAXIS" released from lung by cobra venom or after anaphylactic shock. The relationship between SRS-A leukotrienes was established by UV which showed the presence of the conjugated triene. (From Merck Index, 11th ed)Respiratory Burst: A large increase in oxygen uptake by neutrophils and most types of tissue macrophages through activation of an NADPH-cytochrome b-dependent oxidase that reduces oxygen to a superoxide. Individuals with an inherited defect in which the oxidase that reduces oxygen to superoxide is decreased or absent (GRANULOMATOUS DISEASE, CHRONIC) often die as a result of recurrent bacterial infections.Calcimycin: An ionophorous, polyether antibiotic from Streptomyces chartreusensis. It binds and transports CALCIUM and other divalent cations across membranes and uncouples oxidative phosphorylation while inhibiting ATPase of rat liver mitochondria. The substance is used mostly as a biochemical tool to study the role of divalent cations in various biological systems.Macrophages, Peritoneal: Mononuclear phagocytes derived from bone marrow precursors but resident in the peritoneum.Platelet Activating Factor: A phospholipid derivative formed by PLATELETS; BASOPHILS; NEUTROPHILS; MONOCYTES; and MACROPHAGES. It is a potent platelet aggregating agent and inducer of systemic anaphylactic symptoms, including HYPOTENSION; THROMBOCYTOPENIA; NEUTROPENIA; and BRONCHOCONSTRICTION.Complement C3b: The larger fragment generated from the cleavage of COMPLEMENT C3 by C3 CONVERTASE. It is a constituent of the ALTERNATIVE PATHWAY C3 CONVERTASE (C3bBb), and COMPLEMENT C5 CONVERTASES in both the classical (C4b2a3b) and the alternative (C3bBb3b) pathway. C3b participates in IMMUNE ADHERENCE REACTION and enhances PHAGOCYTOSIS. It can be inactivated (iC3b) or cleaved by various proteases to yield fragments such as COMPLEMENT C3C; COMPLEMENT C3D; C3e; C3f; and C3g.Peritonitis: INFLAMMATION of the PERITONEUM lining the ABDOMINAL CAVITY as the result of infectious, autoimmune, or chemical processes. Primary peritonitis is due to infection of the PERITONEAL CAVITY via hematogenous or lymphatic spread and without intra-abdominal source. Secondary peritonitis arises from the ABDOMINAL CAVITY itself through RUPTURE or ABSCESS of intra-abdominal organs.Complement Pathway, Alternative: Complement activation initiated by the interaction of microbial ANTIGENS with COMPLEMENT C3B. When COMPLEMENT FACTOR B binds to the membrane-bound C3b, COMPLEMENT FACTOR D cleaves it to form alternative C3 CONVERTASE (C3BBB) which, stabilized by COMPLEMENT FACTOR P, is able to cleave multiple COMPLEMENT C3 to form alternative C5 CONVERTASE (C3BBB3B) leading to cleavage of COMPLEMENT C5 and the assembly of COMPLEMENT MEMBRANE ATTACK COMPLEX.Lectins, C-Type: A class of animal lectins that bind to carbohydrate in a calcium-dependent manner. They share a common carbohydrate-binding domain that is structurally distinct from other classes of lectins.Mannose-Binding Lectins: A subclass of lectins that are specific for CARBOHYDRATES that contain MANNOSE.Arachidonic Acid: An unsaturated, essential fatty acid. It is found in animal and human fat as well as in the liver, brain, and glandular organs, and is a constituent of animal phosphatides. It is formed by the synthesis from dietary linoleic acid and is a precursor in the biosynthesis of prostaglandins, thromboxanes, and leukotrienes.Tetradecanoylphorbol Acetate: A phorbol ester found in CROTON OIL with very effective tumor promoting activity. It stimulates the synthesis of both DNA and RNA.Complement Activation: The sequential activation of serum COMPLEMENT PROTEINS to create the COMPLEMENT MEMBRANE ATTACK COMPLEX. Factors initiating complement activation include ANTIGEN-ANTIBODY COMPLEXES, microbial ANTIGENS, or cell surface POLYSACCHARIDES.Complement C3: A glycoprotein that is central in both the classical and the alternative pathway of COMPLEMENT ACTIVATION. C3 can be cleaved into COMPLEMENT C3A and COMPLEMENT C3B, spontaneously at low level or by C3 CONVERTASE at high level. The smaller fragment C3a is an ANAPHYLATOXIN and mediator of local inflammatory process. The larger fragment C3b binds with C3 convertase to form C5 convertase.Nitroblue Tetrazolium: Colorless to yellow dye that is reducible to blue or black formazan crystals by certain cells; formerly used to distinguish between nonbacterial and bacterial diseases, the latter causing neutrophils to reduce the dye; used to confirm diagnosis of chronic granulomatous disease.Properdin: A 53-kDa protein that is a positive regulator of the alternate pathway of complement activation (COMPLEMENT ACTIVATION PATHWAY, ALTERNATIVE). It stabilizes the ALTERNATIVE PATHWAY C3 CONVERTASE (C3bBb) and protects it from rapid inactivation, thus facilitating the cascade of COMPLEMENT ACTIVATION and the formation of MEMBRANE ATTACK COMPLEX. Individuals with mutation in the PFC gene exhibit properdin deficiency and have a high susceptibility to infections.Phagosomes: Membrane-bound cytoplasmic vesicles formed by invagination of phagocytized material. They fuse with lysosomes to form phagolysosomes in which the hydrolytic enzymes of the lysosome digest the phagocytized material.Macrophage-1 Antigen: An adhesion-promoting leukocyte surface membrane heterodimer. The alpha subunit consists of the CD11b ANTIGEN and the beta subunit the CD18 ANTIGEN. The antigen, which is an integrin, functions both as a receptor for complement 3 and in cell-cell and cell-substrate adhesive interactions.Catalogs, LibraryCatalogs as Topic: Ordered compilations of item descriptions and sufficient information to afford access to them.Complement Factor B: A glycine-rich, heat-labile serum glycoprotein that contains a component of the C3 CONVERTASE ALTERNATE PATHWAY (C3bBb). Bb, a serine protease, is generated when factor B is cleaved by COMPLEMENT FACTOR D into Ba and Bb.Agammaglobulinemia: An immunologic deficiency state characterized by an extremely low level of generally all classes of gamma-globulin in the blood.Complement Pathway, Classical: Complement activation initiated by the binding of COMPLEMENT C1 to ANTIGEN-ANTIBODY COMPLEXES at the COMPLEMENT C1Q subunit. This leads to the sequential activation of COMPLEMENT C1R and COMPLEMENT C1S subunits. Activated C1s cleaves COMPLEMENT C4 and COMPLEMENT C2 forming the membrane-bound classical C3 CONVERTASE (C4B2A) and the subsequent C5 CONVERTASE (C4B2A3B) leading to cleavage of COMPLEMENT C5 and the assembly of COMPLEMENT MEMBRANE ATTACK COMPLEX.Electronic Mail: Messages between computer users via COMPUTER COMMUNICATION NETWORKS. This feature duplicates most of the features of paper mail, such as forwarding, multiple copies, and attachments of images and other file types, but with a speed advantage. The term also refers to an individual message sent in this way.Periodicals as Topic: A publication issued at stated, more or less regular, intervals.Journal Impact Factor: A quantitative measure of the frequency on average with which articles in a journal have been cited in a given period of time.Food Dispensers, Automatic: Mechanical food dispensing machines.Pharmacology, Clinical: The branch of pharmacology that deals directly with the effectiveness and safety of drugs in humans.Pharmacology: The study of the origin, nature, properties, and actions of drugs and their effects on living organisms.Publishing: "The business or profession of the commercial production and issuance of literature" (Webster's 3d). It includes the publisher, publication processes, editing and editors. Production may be by conventional printing methods or by electronic publishing.GABA-B Receptor Agonists: Endogenous compounds and drugs that bind to and activate GABA-B RECEPTORS.Receptors, GABA-B: A subset of GABA RECEPTORS that signal through their interaction with HETEROTRIMERIC G-PROTEINS.Baclofen: A GAMMA-AMINOBUTYRIC ACID derivative that is a specific agonist of GABA-B RECEPTORS. It is used in the treatment of MUSCLE SPASTICITY, especially that due to SPINAL CORD INJURIES. Its therapeutic effects result from actions at spinal and supraspinal sites, generally the reduction of excitatory transmission.ArthritisArthritis, Experimental: 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.Nadolol: A non-selective beta-adrenergic antagonist with a long half-life, used in cardiovascular disease to treat arrhythmias, angina pectoris, and hypertension. Nadolol is also used for MIGRAINE DISORDERS and for tremor.Multiple Organ Failure: A progressive condition usually characterized by combined failure of several organs such as the lungs, liver, kidney, along with some clotting mechanisms, usually postinjury or postoperative.Sepsis: 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.Compassionate Use Trials: Providing an investigational therapy to a patient who is not eligible to receive that therapy in a clinical trial, but who has a serious or life-threatening illness for which other treatments are not available. Compassionate use trials allow patients to receive promising but not yet fully studied or approved therapies when no other treatment option exists. Also called expanded access trial.Candidiasis: Infection with a fungus of the genus CANDIDA. It is usually a superficial infection of the moist areas of the body and is generally caused by CANDIDA ALBICANS. (Dorland, 27th ed)Candidemia: A form of invasive candidiasis where species of CANDIDA are present in the blood.Candidiasis, Oral: Infection of the mucous membranes of the mouth by a fungus of the genus CANDIDA. (Dorland, 27th ed)

Activation of stimulus-specific serine esterases (proteases) in the initiation of platelet secretion. I. Demonstration with organophosphorus inhibitors. (1/1146)

The effect of organophosphorus inhibitors of serine esterases (proteases) on secretion from washed rabbit platelets was examined. Five noncytotoxic stimuli were employed: collagen, thrombin, heterologous anti-platelet antibody (in the absence of complement), rabbit C3 bound to zymosan, and platelet activating factor derived from antigen-stimulated, IgE-sensitized rabbit basophils. Diisoprophyl phosphofluoridate, three series of p-nitrophenyl ethyl phosphonates, and a series of cyclohexyl phenylalkylphosphonofluridates were all found to be inhibitory to the platelet secretion. These are irreversible inhibitors of serine proteases but in this system were only inhibitory if added to the platelets concurrently with the stimuli. Pretreatment of either the platelets or the stimuli with the inhibitors followed by washing, was without effect on the subsequent reaction. This suggested the involvement of stimulus-activatable serine proteases in the secretory process. The concept was supported by finding that nonphosphorylating phosphonates or hydrolyzed phosphonates or phosphonofluoridates were without inhibitory action. The effect of a series of phosphonates or phosphonoflouridates in inhibiting each stimulus exhibited a unique activity-structure profile. The demonstration of such unique profiles with four series of inhibitors for each of the five stimuli was interpreted as demonstrating that a specific activatable serine protease was involved in the platelet secretory response to each stimulus.  (+info)

Acidification of the phagosome in Crassostrea virginica hemocytes following engulfment of zymosan. (2/1146)

Phagocytic hemocytes are responsible for engulfing and internally degrading foreign organisms within the hemolymph and tissue of the eastern oyster, Crassostrea virginica. Since rapid acidification of the phagosome lumen is typically essential for activation of hydrolytic and reactive oxygen intermediate (ROI) producing enzymes in vertebrate cells, we measured phagosomal pH in oyster hemocytes by using the emission fluorescence of two fluorescent probes, rhodamine and Oregon Green 488 (OG 488), conjugated to zymosan to determine whether oyster hemocyte phagosomes become acidified after phagocytosis of zymosan. The average pH of 1079 phagosomes within 277 hemocytes 1 h after phagocytosis of zymosan was 3.9 +/- 0.03. Observations of 141 hemocytes with internalized zymosan by light microscopy revealed that, over a 60-min time period, 51% of highly granular hemocytes became partially granular, and 29% became agranular. In addition, 83% of partially granular hemocytes containing zymosan at time = 0 became agranular within 60 min. A comparison revealed that the phagosomes of agranular hemocytes were much more acidic (pH 3.1 +/- 0.02) than those of highly granular hemocytes (4.9 +/- 0.02; P < 0.05). These values are significantly lower than most reported in the literature for blood cells from metazoan organisms.  (+info)

Effect of nitric oxide donors on oxygen-dependent cytotoxic responses mediated by neutrophils. (3/1146)

We analyzed the effect of nitric oxide (NO) on oxygen-dependent cytotoxic responses mediated by neutrophils against unopsonized erythrocytes using three NO donors: S-nitrosoglutathione (GSNO), S-nitroso-N-acetylpenicillamine (SNAP), and sodium nitroprusside (SNP). Neutrophils were treated with these compounds for 1-2 min at 37 degrees C and cytotoxicity was then triggered in the presence of NO donors by precipitating immune complexes, aggregated IgG, the chemotactic peptide FMLP, or opsonized zymosan. GSNO induced, in all cases, a marked increase in cytotoxic responses, while SNAP moderately increased cytotoxicity triggered by immune complexes, aggregated IgG, or Z, opsonized zymosen, without modifying those responses induced by FMLP. By contrast, SNP dramatically suppressed cytotoxicity triggered by all of the stimuli assessed. The enhancing effects mediated by GSNO and SNAP did not depend on the stimulation of guanylyl cyclase and were prevented by the NO scavengers hemoglobin and PTIO (2-phenyl-4,4,5,5-tetramethyl-imidazoline-1-oxyl 3-oxide). The inhibitory activity of SNP, on the other hand, was not prevented by NO scavengers, suggesting that it cannot be ascribed to the release of NO. In another set of experiments, neutrophils were pretreated with GSNO or SNAP for different times. Then cells were washed to remove NO donors from the culture medium, and cytotoxicity was triggered by different stimuli. It was found that neutrophils must be pretreated with NO donors for at least 4 h to increase cytotoxic responses, and pretreatment for longer periods (i.e., 8 or 18 h) further increased cytotoxicity. Not only cytotoxic responses, but also the production of O2- and H2O2, and the release of myeloperoxidase were increased under these conditions.  (+info)

Selective regulation of cytokine induction by adenoviral gene transfer of IkappaBalpha into human macrophages: lipopolysaccharide-induced, but not zymosan-induced, proinflammatory cytokines are inhibited, but IL-10 is nuclear factor-kappaB independent. (4/1146)

Macrophages are the major cytokine producers in chronic inflammatory diseases, but the biochemical pathways regulating cytokine production are poorly understood. This is because genetic tools to dissect signaling pathways cannot be used in macrophages because of difficulties in transfection. We have developed an adenoviral technique to achieve high efficiency gene delivery into macrophages and recently showed that spontaneous TNF-alpha production in rheumatoid arthritis joint cells, chiefly from macrophages, is 75% blocked by adenoviral transfer of IkappaBalpha. In this report we use the same adenovirus to investigate whether the production of a number of proinflammatory cytokines (e.g., TNF-alpha, IL-1beta, IL-6, and IL-8) from human macrophages depends on NF-kappaB. While the cytokine response to certain inducers, such as LPS, PMA, and UV light, is blocked by overexpression of IkappaBalpha, the response to zymosan is not. In contrast, anti-inflammatory mediators (IL-10 and IL-1 receptor antagonist) induced by LPS are only marginally inhibited by IkappaBalpha excess. These studies demonstrate several new points about macrophage cytokine production. First, there is heterogeneity of mechanisms regulating both the proinflammatory and anti-inflammatory cytokines within populations of a single cell type. In addition, the results confirm the utility of the adenoviral technique for functional analysis of cytokine induction. The results also confirm that there are autocrine and paracrine interactions regulating cytokine synthesis within a single cell type. The selectivity of NF-kappaB blockade for proinflammatory but not anti-inflammatory mediators indicates that in macrophages, NF-kappaB may be a good target for the treatment of chronic inflammatory diseases.  (+info)

Extracellular acidification induces human neutrophil activation. (5/1146)

In the current work, we evaluated the effect of extracellular acidification on neutrophil physiology. Neutrophils suspended in bicarbonate-buffered RPMI 1640 medium adjusted to acidic pH values (pH 6.5-7.0) underwent: 1) a rapid transient increase in intracellular free calcium concentration levels; 2) an increase in the forward light scattering properties; and 3) the up-regulation of surface expression of CD18. By contrast, extracellular acidosis was unable to induce neither the production of H2O2 nor the release of myeloperoxidase. Acidic extracellular pH also modulated the functional profile of neutrophils in response to conventional agonists such as FMLP, precipiting immune complexes, and opsonized zymosan. It was found that not only calcium mobilization, shape change response, and up-regulation of CD18 expression but also production of H2O2 and release of myeloperoxidase were markedly enhanced in neutrophils stimulated in acidic pH medium. Moreover, extracellular acidosis significantly delayed neutrophil apoptosis and concomitantly extended neutrophil functional lifespan. Extracellular acidification induced an immediate and abrupt fall in the intracellular pH, which persisted over the 240-s analyzed. A similar abrupt drop in the intracellular pH was detected in cells suspended in bicarbonate-supplemented PBS but not in those suspended in bicarbonate-free PBS. A role for intracellular acidification in neutrophil activation is suggested by the fact that only neutrophils suspended in bicarbonate-buffered media (i.e., RPMI 1640 and bicarbonate-supplemented PBS) underwent significant shape changes in response to extracellular acidification. Together, our results support the notion that extracellular acidosis may intensify acute inflammatory responses by inducing neutrophil activation as well as by delaying spontaneous apoptosis and extending neutrophil functional lifespan.  (+info)

Participation of cofilin in opsonized zymosan-triggered activation of neutrophil-like HL-60 cells through rapid dephosphorylation and translocation to plasma membranes. (6/1146)

We studied the roles of cofilin, an actin-binding phosphoprotein, in superoxide production of neutrophil-like HL-60 cells triggered by opsonized zymosan (OZ). OZ caused dephosphorylation of cofilin as well as a transient increase of F-actin. Both reactions were complete within 30 s. Okadaic acid (OA) magnified the OZ-triggered O2--production 3.3-fold at 1 microM, but inhibited it completely at 5 microM. We used these critical concentrations to study the effects of OA on changes in phosphorylation and intracellular localization of cofilin. The OZ-induced dephosphorylation of cofilin was inhibited by 5 microM OA but not by 1 microM OA. Subcellular fractionation and immunoblotting revealed that 1 microM OA increased cofilin on the phagosomal membranous fraction but 5 microM OA decreased it. At 1 microM, OA increased translocation of p47phox to membranes, which may explain in part the enhancing effect of 1 microM OA. Confocal laser scanning microscopy showed that: (i) Cofilin diffused throughout the cytosol of resting cells, but accumulated at the plasma membranes forming phagocytic vesicles in activated cells. (ii) At 1 microM, OA had little effect on the OZ-evoked translocation of cofilin, whereas 5 microM OA suppressed it completely. (iii) OA alone, which could not trigger the phagocytic respiratory burst, did not cause any change in the distribution of cofilin at such concentrations. Furthermore, in a superoxide-producing cell-free system employing membranous and cytosolic fractions, affinity-purified anti-cofilin antibody showed an enhancing effect. These results suggest that cofilin participates in the superoxide production of the OZ-activated phagocytes through dephosphorylation and translocation. The roles of cofilin in the activated leukocytes will be discussed.  (+info)

Roles of a macrophage receptor with collagenous structure (MARCO) in host defense and heterogeneity of splenic marginal zone macrophages. (7/1146)

Class A type I and type II macrophage scavenger receptors (MSR-A) and a macrophage receptor with collagenous structure (MARCO) are trimeric membrane glycoproteins mediating the uptake of chemically modified low density lipoproteins. MSR-A is expressed constitutively in several tissue macrophages and in liver sinusoidal endothelial cells, whereas MARCO is expressed constitutively in splenic marginal zone macrophages and in macrophages and endothelial cells in the lymphatic medullary sinuses of lymph nodes. The administration of LPS, zymosan, BCG, or L. monocytogenes to mice resulted in marked and transient MARCO expression and in the upregulation of MSR-A expression in the liver and spleen. In osteopetrotic (op) mutant mice defective in the production on M-CSF, ER-TR9-positive marginal zone macrophages and MOMA-1-positive marginal metallophilic macrophages were absent, whereas MARCO-expressing marginal zone macrophages were present, indicating the heterogeneity of marginal zone macrophages. Intravenous administration of BCG resulted in marked accumulation of BCG bacilli in the both marginal zone macrophages and marginal metallophilic macrophages in littermate control mice. In contrast, BCG bacilli were incorporated almost exclusively by MARCO-expressing marginal zone macrophages in op/op mice. These results indicate that MARCO is not only expressed constitutively in specific macrophage subpopulations but is also induced by various bacterial antigens and plays a role in host defense against bacteria.  (+info)

Phospholipase D-derived phosphatidic acid is involved in the activation of the CD11b/CD18 integrin in human eosinophils. (8/1146)

Priming of human eosinophils is an essential event for the respiratory burst induced by serum-opsonized particles [serum-treated zymosan (STZ)]. In this study we have found that treatment of eosinophils with platelet-activating factor (PAF) leads to activation of phospholipase D. Inhibition of the formation of phospholipase D-derived products by ethanol resulted in about 90% inhibition of PAF-induced binding of fluorescent STZ particles to the cells, but only when ethanol was added to the cells before treatment with PAF. When ethanol was added after treatment with PAF, only a minor inhibition of the STZ binding and STZ-induced response was observed. These results indicate that phospholipase D-derived phosphatidic acid is involved in PAF priming, without having an effect on STZ stimulation. In the presence of propranolol, which inhibits phosphatidic acid-phosphatase activity, binding of STZ particles to human eosinophils induced by suboptimal concentrations of PAF was enhanced, indicating that phosphatidic acid and not diradylglyceride is the relevant molecule derived from phospholipase D activity. Addition of cell-permeant diC8-phosphatidic acid (DiC8-PA) to human eosinophils resulted in CD11b/CD18-dependent adhesion, both to STZ particles and fibronectin-coated wells, without significant upregulation of CD11b/CD18. The DiC8-PA-induced adhesion was not mediated via the fatty acid moiety, because other C8-lipids such as 1,2-diC8-phosphatidylcholine, 1-C8-monoacylglycerol or C8-ceramide were without effect. Activation of protein kinase C with PMA or 1,2-diC8-diacylglycerol did result in enhanced STZ binding. However, under these latter conditions upregulation of CD11b/CD18 was observed. Taken together, these results suggest that phospholipase D-derived PA is involved in changing the affinity of the CD11b/CD18 integrin for its ligands.  (+info)

  • In plasma, most metabolites in the central metabolic pathway (glycolysis and TCA cycle) were significantly downregulated after zymosan administration. (elsevier.com)
  • In PWF, most of metabolites that could detected increased in zymosan-treated mice, which is suggestive of inflammation, oxidative stress and increased energy demands. (elsevier.com)
  • Significant and time-dependent changes in metabolite profiles after zymosan administration were observed in both peritoneal wash fluid (PWF) and plasma. (elsevier.com)
  • In macrophages, zymosan-induced responses include the induction of proinflammatory cytokines, arachidonate mobilization, protein phosphorylation, and inositol phosphate formation. (wikipedia.org)
  • The resulting conjugate, zymosan-FF6, was ingested by macrophages and its fluorescence emission was recorded in situ after phagocytosis, using digital imaging. (nih.gov)
  • We have examined the effects of various mannans, glycoproteins, oligosaccharides, monosaccharides, and sugar phosphates on the binding and phagocytosis of yeast cell walls (zymosan) by mouse peritoneal macrophages. (columbia.edu)
  • The binding and ingestion of zymosan but not of IgG- or complement-coated erythrocytes can be obliterated by plating macrophages on substrates coated with poly-L-lysin (PLL)-mannan. (columbia.edu)
  • Zymosan uptake was completely abolished by trypsin treatment of the macrophages and reduced by 50-60 percent in the presence of 10 mM EGTA. (columbia.edu)
  • Pretreatment of the macrophages with chloroquine inhibited zymosan binding and ingestion. (columbia.edu)
  • Here, using novel and specific reagents, we have defined the receptors involved in the nonopsonic recognition of zymosan and soluble β-glucans in primary macrophages. (rupress.org)
  • However, secretion of PGE2 by tissue-fixed macrophages from within the colorectal carcinomata in response to opsonised zymosan was significantly higher than in the uninvolved colonic tissue. (nih.gov)
  • Leukotriene B4 secretion by intestinal macrophages in response to opsonised zymosan was not significantly elevated in the colonic tumour tissue. (nih.gov)
  • Injections with zymosan can promote macrophages to enter the eye and secrete oncomodulin. (wikipedia.org)
  • Suspensions of alveolar macrophages obtained from male Sprague-Dawley-rats were stimulated with 0 to 3000 micrograms per milliliter (microg/ml) concanavalin-A (11028710) (conA) or 0 to 6.0mg/ml zymosan (9010724) particles. (cdc.gov)
  • Additionally rat alveolar macrophages were preincubated with 0 or 0.12 millimolar cytochrome-c (9007436), followed by 0.1 to 2.0mg/ml zymosan. (cdc.gov)
  • Rat alveolar macrophages were treated with 0 or 0.1mg/ml zymosan and 0 or 5microg/ml cytochalasin-B (14930962). (cdc.gov)
  • In order to determine the possible role of cyclooxygenases and lipoxygenases in the activation of macrophages by LPS, the effects of several inhibitors of these enzymes on the binding and uptake of zymosan particles by macrophages primed with LPS was investigated and a lipoxygenase product, 13-hydroxyoctadecadienoic acid (13-HODD) was isolated from activated cells. (springer.com)
  • Triplelux-A examines immune cells called macrophages from rats to see how they respond to Zymosan. (esa.int)
  • Whereas the control complement (C)-opsonized particle zymosan (COZ) induced a 4.6-fold increase in ¿Ca(2+)(c) in human macrophages, no change in ¿Ca(2+)(c) occurred upon addition of live, C-opsonized virulent M. tuberculosis. (nih.gov)
  • The mRNA and protein expression levels of type I (IFN-α/β) and II (IFN-γ) IFNs, as well as of related downstream inflammatory cytokines (interleukin (IL)-1α, IL-6, IL-12, and IL-17), were detected in macrophages, neutrophils, lymphocytes, and corneal epithelial cells (A6(1) cells) stimulated with zymosan (10 mg/ml) for 8 or 24 h. (molvis.org)
  • Zymosan, a yeast cell wall preparation that binds activated forms of complement C3, is a useful model target to activate the complement system. (elsevier.com)
  • The objective was to evaluate the adjuvant effect of zymosan, a crude yeast cell wall preparation of 1-->3-ß-glucan, during ovalbumin (OVA) sensitization in an allergy model. (cdc.gov)
  • Bovine serum, pre-treated with a yeast cell wall preparation (zymosan), was infused into one half of the mammary gland of 8 cows shortly after dry off. (usda.gov)
  • Treating serum with zymosan (yeast cell wall preparation) causes complement to cleave, allowing this serum to serve as a source of C5a, a potent chemo-attractant and activator of the immune system. (usda.gov)
  • The activity is specific in that the eluate from zymosan fails to enhance C3 and B depletion in H gamma S or absorbed NHS by lipopolysaccharide or Sepharose. (jimmunol.org)
  • Immunohistochemical examination demonstrated a marked increase in the immunoreactivity to nitrotyrosine, a specific "footprint" of peroxynitrite, in the lung of zymosan-shocked rats. (nih.gov)
  • Pretreatment of zymosan-shocked rats with ip administration of N-acetylcysteine (40, 20, and 10 mg/kg, 1 and 6 hrs after zymosan) prevented the development of peritonitis and reduced peroxynitrite formation in a dose-dependent manner. (nih.gov)
  • We evaluated A. esculentus lectin (AEL) efficacy in reducing zymosan-induced temporomandibular joint inflammatory hypernociception in rats along with the mechanism of action through which it exerts anti-inflammatory activity. (ovid.com)
  • Results: Zymosan induced obvious inflammatory morphology and functional impairment in the essential organs in the rats, which is indicative of characteristic changes in the MOF. (paper.edu.cn)
  • To address these discrepancies, we assessed the differential role of IL-17 pathway in two models of fungal sepsis: intravenous infection with live Candida albicans , in which fungal growth is the main cause of mortality, and zymosan-induced multiple organ failure in which the inflammatory pathology drives the mortality. (biomedcentral.com)
  • IL-17RA -/- and control mice were also assessed for mortality in a multiorgan failure sepsis model induced by the fungal component zymosan. (biomedcentral.com)
  • Finally, globally NADPH oxidase-deficient mice developed exuberant neutrophilic lung inflammation and proinflammatory cytokine responses to zymosan, a fungal cell wall-derived product composed principally of particulate β-glucans, whereas inflammation in transgenic and wild-type mice was mild and transient. (jimmunol.org)
  • This BioParticles® product line consists of a series of fluorescently labeled killed bacteria and yeast (zymosan), offering a variety of sizes, shapes, and natural antigenicities. (thermofisher.com)
  • In this experiment, leukocytes will be observed as they ingest a safer stand-in for bacteria called Zymosan, a harmless molecule that triggers similar immune responses. (esa.int)
  • Zymosan is a ligand found on the surface of fungi, like yeast. (wikipedia.org)
  • In the present study, we investigated the anti-inflammatory effects of PPAR-beta/delta activation, through the use of GW0742 (0,3 mg/kg 10% Dimethyl sulfoxide (DMSO) i.p), a synthetic high affinity ligand, on the development of zymosan-induced multiple organ failure (MOF). (unime.it)
  • Sigma-Aldrich does not measure the particle size of zymosan. (sigmaaldrich.com)
  • Zymosan is a β-glucan- and mannan-rich particle that is widely used as a cellular activator for examining the numerous responses effected by phagocytes. (rupress.org)
  • Zymosan is a yeast-derived particle composed principally of polysaccharides, of which β-glucan, the active component mediating the cellular effects ( 2 ), and mannan are the major constituents ( 3 ). (rupress.org)
  • In vivo administration of zymosan, or purified soluble β-glucans, has a number of desirable effects on immune function, including the ability to confer resistance to tumors and various infections, prompting interest in the development of β-glucan-based therapeutics ( 4 , 5 ). (rupress.org)
  • In vivo challenge with the yeast cell wall product zymosan rapidly induced IL-17 production in these cells. (rupress.org)
  • Interestingly, the yeast wall product zymosan elicited IL-17 production by LTi-like cells in vivo. (rupress.org)
  • Elevations were observed in lung neutrophils, TNF-a, and parameters of lung injury in the groups primed with both zymosan and OVA. (cdc.gov)
  • This treatment succeeded in activating both neutrophils and lymphocytes as evidenced by the expression of IFN-g and IL-8 in the cells obtained from the zymosan serum-infused quarters vs. saline infused quarters. (usda.gov)
  • Our hypothesis was that intramammary infusion of zymosan-treated serum (ZTS) would recruit neutrophils and generate prolonged activity in lymphocytes within the mammary gland. (usda.gov)
  • An acid eluate from the zymosan restores the defect of absorbed NHS and C2D, and also enhances C3 and factor B utilization in hypogammaglobulinemic serum (H gamma S) in a dose-dependent fashion. (jimmunol.org)
  • A b-LF dose of 5 mg/mouse/day reduced the zymosan-induced joint swelling without modulating inflammatory cell infiltration and cartilage proteoglycan depletion. (ru.nl)
  • The PPAR-beta/delta agonist, GW0742, at the dose of 0,3 mg/kg in 10% DMSO, also attenuated the multiple organ dysfunction syndrome caused by zymosan. (unime.it)
  • The time course and dose response curves for zymosan and conA stimulated oxygen consumption did not match those for hydrogen- peroxide and O2- production. (cdc.gov)
  • In nearly all parameters, a non-linear dose-response relationship was observed in the groups primed with OVA and zymosan. (cdc.gov)
  • The optimum adjuvant dose of zymosan was 10 µg. (cdc.gov)
  • On the other hand, the absence of IL-17RA in the knockout mice did not protect the mice against the multiorgan failure induced by zymosan. (biomedcentral.com)
  • Combination therapy of cyclophosphamide and zymosan on a spontaneous mammary cancer in mice. (jax.org)
  • Methods: Multiple organ failure (MOF) was induced in mice by administration of zymosan (given at 500 mg/kg, i.p. as a suspension in saline). (unime.it)
  • MOF and systemic inflammation in mice was assessed 18 hours after administration of zymosan. (unime.it)
  • In pancreas, lung and gut, immunohistochemical analysis of some end points of the inflammatory response, such as inducible nitric oxide synthase (iNOS), nitrotyrosine, poly (ADP-ribose) (PAR), TNF- and IL-1as well as FasL, Bax, Bcl-2 and apoptosis, revealed positive staining in sections of tissue obtained from zymosan-injected mice. (unime.it)
  • On the contrary, these parameters were markedly reduced in samples obtained from mice treated with GW0742 Conclusions: In this study, we have shown that GW0742 attenuates the degree of zymosan-induced non-septic shock in mice. (unime.it)
  • BALB/c mice were sensitized by pharyngeal aspiration with saline, 50 µg of OVA, or OVA with 1, 10, 50, or 75 µg of zymosan on days 0, 7, and 14. (cdc.gov)
  • This study demonstrated an adjuvant effect of zymosan when exposures occurred during the sensitization phase in an OVA-induced allergy model in BALB/c mice. (cdc.gov)
  • Early studies, using carbohydrate inhibitors to block various leukocyte receptors, suggested that the cellular recognition of unopsonized zymosan is mediated by the mannose receptor and a β-glucan receptor ( 6 - 8 ). (rupress.org)
  • Information on preparation of zymosan for use in a properdin assay, which includes boiling zymosan suspensions, is described on theproduct information sheet (under Documents, above). (sigmaaldrich.com)
  • A gel shift assay was used to examine the DNA-binding activity of NFkB in the zymosan A- treated cells. (cdc.gov)
  • We have developed a no-wash, no-quench assay for phagocytosis using Esherichia coli , Staphylococcus aureus , or yeast zymosan conjugated to the pHrodo™ Red or Green indicators ( Figure 3 ). (thermofisher.com)
  • Exudate formation, leukocyte infiltration, nitrate/nitrite production, lung and intestine myeloperoxidase activity and lipid peroxidation, and histologic examination were evaluated at 18 hrs after zymosan administration. (nih.gov)
  • The present study used zymosan A-induced tumor necrosis factor (TNF)-alpha production as a model to explore the signal transduction pathway for B-glucan stimulation in RAW264.7 cells. (cdc.gov)
  • The mRNA and protein expression levels of inflammatory cytokines (IL-1α, IL-6, IL-12, and IL-17) were also upregulated after zymosan stimulation. (molvis.org)
  • Activity of compounds was investigated by looking their influence on oxidative burst activity of zymosan stimulated whole blood phagocytes by using a luminol enhanced chemiluminescence technique. (thefreedictionary.com)
  • In a zymosan-induced ear-skin inflammation model both components decreased the inflammatory response locally (ear swelling and inflammatory cytokine concentration in the ears) and systemically (number of TNF-alpha producing spleen cells). (ru.nl)
  • CONCLUSION: Tyrphostin AG-490 reduced the magnitude of the initial inflammatory response in zymosan-induced shock and prevented the development of severe kidney dysfunction. (msu.ru)
  • The drug diminished the production of zymosan-specific IgG antibodies and hindered the glomeruli from IgGs recognition. (msu.ru)
  • In the present study, we evaluated the effect of N-acetylcysteine treatment in a nonseptic shock model induced by zymosan in the rat. (nih.gov)
  • Adjuvant effect of zymosan after pulmonary treatment in a mouse ovalbumin allergy model. (cdc.gov)
  • Zymosan is prepared from yeast cell wall and consists of protein-carbohydrate complexes. (wikipedia.org)
  • 2003). "Direct binding of Toll-like receptor 2 to zymosan, and zymosan-induced NF-kappa B activation and TNF-alpha secretion are down-regulated by lung collectin surfactant protein A". J. Immunol. (wikipedia.org)
  • In our trial to analyze C3 diversity in Nile tilapia at the protein level using zymosan, we found that a novel 240-kDa serum protein (ZBP-240) also bound to zymosan in addition to C3-derived fragments. (elsevier.com)
  • Anti-inflammatory effects of orally ingested lactoferrin and glycine in different zymosan-induced inflammation models: evidence for synergistic activity. (ru.nl)
  • A combination of glycine and lactoferrin demonstrated a synergistic anti-inflammatory effect on zymosan-induced skin inflammation and an enhanced decrease in the number of TNF-alpha producing spleen cells compared to the effect of the single components. (ru.nl)
  • In a study on rainbow trout Roher and his co-workers (2011) showed that LPS and zymosan are major inducers of TNF-a secretion, although this secretion is not initially associated with the induction of mRNA expression of TNF-a. (thefreedictionary.com)
  • Inhibition of zymosan-induced kidney dysfunction by tyrphostin AG-490. (msu.ru)
  • RESULTS: Tyrphostin AG-490 attenuated the early phase of zymosan-induced shock via inhibition of MIP-1alpha, RANTES and C5a plasma levels and via elevation of IL-10 in plasma. (msu.ru)
  • Zymosan A also raises cyclin D2 levels suggesting a role for the latter in macrophage activation besides proliferation. (wikipedia.org)
  • I. Human IgG with specificity for Zymosan enhances alternative pathway activation by zymosan. (jimmunol.org)
  • In plasma, most metabolites in the central metabolic pathway (glycolysis and TCA cycle) were significantly downregulated after zymosan administration. (elsevier.com)
  • The above results suggest that activation of NFkB is one of the pathways involved in zymosan A-induced TNF-alpha production. (cdc.gov)
  • Prior absorption of normal human serum (NHS) or C2-deficient human serum (C2D) with zymosan at 0 degrees C results in diminished consumption of C3 and factor B during subsequent incubation of the sera in Mg-EGTA buffer with zymosan at 37 degrees C for 30 min. (jimmunol.org)
  • Zymosan A increased TNF-alpha production in RAW264.7 cells in a time and concentration dependent pattern with the optimal time and concentration occurring at 23 hr and 100 ug/mL zymosan A, respectively. (cdc.gov)
  • A combination of b-LF 0.1 mg/mouse/day and glycine 20 or 50 mg/mouse/day counteracted the zymosan-induced ear swelling synergistically and enhanced the decrease in the number of TNF-alpha producing spleen cells of the individual components. (ru.nl)
  • Genetiska modeller i musen samt farmakologi data stödjer en nyckelroll i T-celler, T-cells beroende autoimmunitet och B-cells lymfom inställningar 3 , 4 . (jove.com)
  • I lymfocyter, MALT1 paracaspase aktivering sker vid montering av en CARD11-BCL10-MALT1 komplexa 5 , som utlöses av antigen-receptor proximala signalering nedströms av T - eller B-cells receptor. (jove.com)
  • Protective effects of poly (ADP-ribose) synthase inhibitors in zymosan-activated plasma induced paw edema. (nih.gov)
Inflammation and Resolution Are Associated with Upregulation of Fatty Acid β-Oxidation in Zymosan-Induced Peritonitis<...
Inflammation and Resolution Are Associated with Upregulation of Fatty Acid β-Oxidation in Zymosan-Induced Peritonitis<... (keio.pure.elsevier.com)
MerTK cleavage limits proresolving mediator biosynthesis and exacerbates tissue inflammation | PNAS
MerTK cleavage limits proresolving mediator biosynthesis and exacerbates tissue inflammation | PNAS (pnas.org)
An Evaluation of the Role of Properdin in Alternative Pathway Activation on Neisseria meningitidis and Neisseria gonorrhoeae |...
An Evaluation of the Role of Properdin in Alternative Pathway Activation on Neisseria meningitidis and Neisseria gonorrhoeae |... (jimmunol.org)
Type 1 and Type 2 Cytokine Regulation of Macrophage Endocytosis: Differential Activation by IL-4/IL-13 as Opposed to IFN-γ or...
Type 1 and Type 2 Cytokine Regulation of Macrophage Endocytosis: Differential Activation by IL-4/IL-13 as Opposed to IFN-γ or... (jimmunol.org)
The Protein Kinase IKKε Is a Potential Target for the Treatment of Inflammatory Hyperalgesia | The Journal of Immunology
The Protein Kinase IKKε Is a Potential Target for the Treatment of Inflammatory Hyperalgesia | The Journal of Immunology (jimmunol.org)
Dectin-1 Is A Major β-Glucan Receptor On Macrophages | JEM
Dectin-1 Is A Major β-Glucan Receptor On Macrophages | JEM (jem.rupress.org)
Plus it
Plus it (jpet.aspetjournals.org)
Immunosuppression via adenosine receptor activation by adenosine monophosphate released from apoptotic cells | eLife
Immunosuppression via adenosine receptor activation by adenosine monophosphate released from apoptotic cells | eLife (elifesciences.org)
JCI -
Maresin 1 activates LGR6 receptor promoting phagocyte immunoresolvent functions
JCI - Maresin 1 activates LGR6 receptor promoting phagocyte immunoresolvent functions (jci.org)
Lymphoid tissue inducer-like cells are an innate source of IL-17 and IL-22 | JEM
Lymphoid tissue inducer-like cells are an innate source of IL-17 and IL-22 | JEM (jem.rupress.org)
Pivotal Role of Reactive Oxygen Species in Differential Regulation of Lipopolysaccharide-Induced Prostaglandins Production in...
Pivotal Role of Reactive Oxygen Species in Differential Regulation of Lipopolysaccharide-Induced Prostaglandins Production in... (molpharm.aspetjournals.org)
Differential Ability of Exogenous Chemotactic Agents to Disrupt Transendothelial Migration of Flowing Neutrophils | The Journal...
Differential Ability of Exogenous Chemotactic Agents to Disrupt Transendothelial Migration of Flowing Neutrophils | The Journal... (jimmunol.org)
Relative Contribution of LFA-1 and Mac-1 to Neutrophil Adhesion and Migration | The Journal of Immunology
Relative Contribution of LFA-1 and Mac-1 to Neutrophil Adhesion and Migration | The Journal of Immunology (jimmunol.org)
Novel Resolvin D2 Receptor Axis in Infectious Inflammation | The Journal of Immunology
Novel Resolvin D2 Receptor Axis in Infectious Inflammation | The Journal of Immunology (jimmunol.org)
JCI -
Volume 91, Issue 4
JCI - Volume 91, Issue 4 (jci.org)
Expression and Function of the Chemokine Receptors CXCR1 and CXCR2 in Sepsis | The Journal of Immunology
Expression and Function of the Chemokine Receptors CXCR1 and CXCR2 in Sepsis | The Journal of Immunology (jimmunol.org)
In vivo Pain models and pain studies | Charles River
In vivo Pain models and pain studies | Charles River (criver.com)
Non-Steroidal Anti-Inflammatory Drugs NSAIDs | GreenMedInfo | Toxic
Non-Steroidal Anti-Inflammatory Drugs NSAIDs | GreenMedInfo | Toxic (greenmedinfo.com)
Host-based lipid inflammation drives pathogenesis in Francisella infection | PNAS
Host-based lipid inflammation drives pathogenesis in Francisella infection | PNAS (pnas.org)
Myeloid Innate Signaling Pathway Regulation by MALT1 Paracaspase Activity | Protocol (Translated to Swedish)
Myeloid Innate Signaling Pathway Regulation by MALT1 Paracaspase Activity | Protocol (Translated to Swedish) (jove.com)
Frontiers | An Organismal Model for Gene Regulatory Networks in the Gut-Associated Immune Response | Immunology
Frontiers | An Organismal Model for Gene Regulatory Networks in the Gut-Associated Immune Response | Immunology (frontiersin.org)
Transcript</b>
Transcript</b> (npr.org)
NIOSHTIC-2  Publications Search - 00175531 - Chemiluminescence associated with phagocytosis of foreign particles in rabbit...
NIOSHTIC-2 Publications Search - 00175531 - Chemiluminescence associated with phagocytosis of foreign particles in rabbit... (cdc.gov)
Activation of mouse peritoneal macrophages and of the alternative pathway of the complement system by cartilage specific...
Activation of mouse peritoneal macrophages and of the alternative pathway of the complement system by cartilage specific... (rd.springer.com)
IL-12 Is Dysregulated in Macrophages from IRF-1 and IRF-2 Knockout Mice | The Journal of Immunology
IL-12 Is Dysregulated in Macrophages from IRF-1 and IRF-2 Knockout Mice | The Journal of Immunology (jimmunol.org)
Pain Reduces Sexual Motivation in Female But Not Male Mice | Journal of Neuroscience
Pain Reduces Sexual Motivation in Female But Not Male Mice | Journal of Neuroscience (jneurosci.org)
Plus it
Plus it (jneurosci.org)
The Effects of Complement Activation on Platelets | Springer for Research & Development
The Effects of Complement Activation on Platelets | Springer for Research & Development (rd.springer.com)
Connexin43 Is Dispensable for Phagocytosis | The Journal of Immunology
Connexin43 Is Dispensable for Phagocytosis | The Journal of Immunology (jimmunol.org)
February 1999 - Volume 11 - Issue 2 : Shock
February 1999 - Volume 11 - Issue 2 : Shock (journals.lww.com)