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PubMed2003

Rifampicin and dexamethasone have similar effects on macrophage phagocytosis of zymosan, but differ in their effects on nitrite and TNF-alpha production.

The antibiotic rifampicin is used extensively in the treatment of mycobacterial and other infections. It has previously been suggested that rifampicin binds to and activates the glucocorticoid receptor potentially leading to pharmacological glucocorticoid-like effects such as host immunosuppression (Calleja et al.). This study compares the effects of rifampicin with the synthetic glucocorticoid dexamethasone, on macrophage phagocytosis of zymosan particles and production of nitric oxide (NO) and tumour necrosis factor-alpha (TNF-alpha) by splenocytes or macrophages. Rifampicin and dexamethasone, partially suppressed zymosan phagocytosis by macrophages, respectively, and both effects were ameliorated by the glucocorticoid receptor antagonist RU486. In other experiments, rifampicin had no effects on NO responses; however, dexamethasone inhibited NO in an RU486-sensitive manner. At high doses, rifampicin moderately suppressed TNF-alpha while dexamethasone inhibited it in a dose-dependent manner, which was ameliorated by the presence of RU486. These findings suggest that rifampicin has differential immunomodulatory effects on these innate immune mechanisms.

Adjuvants, Immunologic↗
PubMed2001

Lipopolysaccharide (LPS) and zymosan-resistant mutant isolated from a macrophage-like cell line, WEHI-3, with a defective response to LPS under serum-free conditions.

A LPS-resistant mutant, W3SF-1, was isolated from a murine macrophage-like cell line, WEHI-3. The W3SF-1 mutant did not produce a significant amount of nitric oxide (NO) or TNF-alpha even with high concentrations of LPS in the presence or absence of FCS, whereas the parental WEHI-3 cells produced them in response to LPS. The parental cells expressed a significant level of TNF-alpha mRNA after LPS stimulation, whereas the mutant cells did not. This defective response of the mutant cells to LPS was neither dependent on the concentration or chemical structure of LPS, nor on the time of LPS treatment. The mutant cells also showed a defective response to zymosan, suggesting that the defect in the mutant cells is common to LPS and zymosan in the signal transduction pathways. The parental and mutant cells showed similar levels of Mac1, F4/80 and CD14, suggesting that these surface markers of macrophages are not linked directly to the defective responses of the mutant to LPS. The treatment of mutant cells with IFN-gamma did not restore the defect of NO or TNF-alpha production on LPS treatment. Binding experiments with 125I-labelled LPS showed a similar binding affinity for LPS in the parental and the mutant cells. These results suggest that the defect in the W3SF-1 mutant cells may not reside in the LPS binding but rather in the early step of signal transduction pathways in the cells after LPS binding.

Animals↗
PubMed1995

MacMARCKS mutation blocks macrophage phagocytosis of zymosan.

A major protein kinase C substrate, MacMARCKS (F52, MPR), was examined for its role in phagocytosis. In macrophage-phagocytosing zymosan particles, MacMARCKS was concentrated around nascent phagosomes as detected by immunofluorescent microscopy. The effector domain of MacMARCKS contains the phosphorylation sites, a calmodulin binding site, as well as a putative actin binding site. Stable J774 macrophage cell lines constitutively expressing effector domain deletion mutants of MacMARCKS were generated. When given zymosan particles, these transfectants showed approximately a 90% reduction in their phagocytic capacity. The receptor-mediated endocytosis of acetylated low density lipoproteins, however, was not affected by the mutant. These results strongly suggest the involvement of MacMARCKS in macrophage phagocytosis.

Cell Adhesion Molecules↗
PubMed2004

Role of group V phospholipase A2 in zymosan-induced eicosanoid generation and vascular permeability revealed by targeted gene disruption.

Conclusions regarding the contribution of low molecular weight secretory phospholipase A2 (sPLA2) enzymes in eicosanoid generation have relied on data obtained from transfected cells or the use of inhibitors that fail to discriminate between individual members of the large family of mammalian sPLA2 enzymes. To elucidate the role of group V sPLA2, we used targeted gene disruption to generate mice lacking this enzyme. Zymosan-induced generation of leukotriene C4 and prostaglandin E2 was attenuated approximately 50% in peritoneal macrophages from group V sPLA2-null mice compared with macrophages from wild-type littermates. Furthermore, the early phase of plasma exudation in response to intraperitoneal injection of zymosan and the accompanying in vivo generation of cysteinyl leukotrienes were markedly attenuated in group V sPLA2-null mice compared with wild-type controls. These data provide clear evidence of a role for group V sPLA2 in regulating eicosanoid generation in response to an acute innate stimulus of the immune response both in vitro and in vivo, suggesting a role for this enzyme in innate immunity.

Animals↗
PubMed2004

Zymosan-induced luminol-dependent chemiluminescence response of circulating and extravasated leukocytes in experimental sepsis.

This study examines a concurrent profiling of circulating and extravasated polymorphonuclear leukocytes (PMNs) in a rat model of experimental sepsis. Fecal peritonitis was induced in Wistar male rats by intraperitoneal instillation of a fecal suspension in saline (1:1 w/v). Blood and peritoneal fluid were collected 8 h following fecal inoculation for the evaluation of inflammatory response of PMNs using zymosan-induced luminol-dependent chemiluminescence. Fifty microliters of pre-diluted blood or peritoneal fluid samples were mixed with 150 microl of reaction mixture (4 x 10(-4) M luminol+50 microg opsonized zymosan+0.1% gelatin in Hank's balanced salt solution) and the chemiluminescence signal was measured in a luminometer at 37 degrees C. Fecal peritonitis caused a significant leukocytopenia (3540+/-297 mm(-3) versus control value of 7525+/-711 mm(-3), p < 0.001) accompanied by massive infiltration of PMNs in the peritoneal cavity (34700+/-4006 versus 7325+/-425 mm(-3), p < 0.001). The phagocytic activity of circulating blood PMNs was down-regulated whereas a significant up-regulation was observed in the activity of PMNs from peritoneal fluid. In conclusion, this study clearly demonstrates sepsis-induced alterations in both blood and peritoneal fluid PMNs and their quantitative assessment may be helpful in disease evaluation and designing effective therapies.

Animals↗
PubMed1957

Quantitative studies on the properdin-complement system. II. Kinetics of the reaction between properdin and zymosan.

The reaction of human, bovine, and pig properdin with excess zymosan exhibits an induction period followed by a rapidly accelerating formation of the properdin-zymosan (PZ) complex. Two methods for determining the quantity of PZ complex are given, one using human serum lacking properdin, the other using a fraction of pig serum containing complement components, C'1, C'3 and C'4.

Animals↗
PubMed1996

Exocytosis of arginine-specific ADP-ribosyltransferase and p33 induced by A23187 and calcium or serum-opsonized zymosan in chicken polymorphonuclear leukocytes.

Exocytosis is a common phenomenon in neutrophil functions. We earlier reported the co-localization of arginine-specific ADP-ribosyltransferase [EC 2.4.2.31] and its target protein p33 (mim-1 protein) in cytoplasmic granules in chicken polymorphonuclear leukocytes (so-called heterophils) [Mishima, K., Terashima, M., Obara, S., Yamada, K., Imai, K., and Shimoyama, M. (1991) J. Biochem. 110, 388-394]. In the present study, we obtained evidence that the transferase and p33 were released into the extracellular space by the stimulus of calcium ionophore A23187 or serum-opsonized zymosan, but scarcely by phorbol myristate acetate (PMA) or N-formyl-Met-Leu-Phe (fMLP), thereby indicating the co-localization of the transferase and p33 in the azurophilic granules, and not in specific granules. [32P]ADP-ribosylation of p33 occurred in the extracellular space, induced by the stimulus of A23187 or opsonized zymosan in the presence of [32P]NAD. Our findings are interpreted to mean that heterophil transferase and p33 may be involved in neutrophil functions during processes of inflammation.

ADP Ribose Transferases↗
PubMed1993

Dynamics and participation of type II phospholipase A2 in rat zymosan-induced pleurisy.

Intrapleural injection of zymosan into rats induces acute inflammation characterized by plasma leakage and cellular influx. The level of type II phospholipase A2 (PLA2) increased in the pleural fluid as well as in exudating leukocytes after the injection of zymosan. Rather low PLA2 activity was found in cell lysates, though treatment of such lysates at low pH increased the PLA2 activity drastically. The appearance of "acid-extracted" PLA2 activity in leukocytes preceded that of the extracellular enzyme activity, suggesting that pleural leukocytes might be one of the origins of the extracellular enzyme. Treatment of exudating pleural leukocytes with purified rat type II PLA2 elicited the production of prostaglandin E2, but not platelet-activating factor appreciably. These findings indicate that type II PLA2 might play a role in the progression of inflammation through the production of eicosanoids in the present inflammation model.

Animals↗
PubMed2001

The effects of lidocaine on superoxide production and p47 Phox translocation in opsonized zymosan-activated neutrophils.

UNLABELLED: Superoxide is generated by reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase that exists in the cell membrane of neutrophils and contains p47 phox in the enzyme complex. Superoxide is closely related to various diseases, including infection, myocardial infarction, and aspiration pneumonia. Therefore we performed this study to establish how lidocaine acts on NADPH oxidase. We examined the effects of lidocaine on superoxide production in neutrophils using the method of 2-methyl-6-phenyl-3,7-dihydro [1,2-a] pyrazin-3-one (CLA phenyl)-dependent chemiluminescence activated by opsonized zymosan (OZ). Treatment with lidocaine 15 microM suppressed OZ-activated CLA phenyl-dependent chemiluminescence by approximately 40% compared with that of OZ only-activated neutrophils. It was further demonstrated that the suppressive effect of lidocaine on superoxide production was dependent on the concentration of lidocaine. Translocation of p47 phox from the cytosol to the cell membrane was studied using immunoblot analysis with a polyclonal anti-p47 phox antibody. Lidocaine suppressed OZ-induced p47 phox translocation in a dose-dependent manner. Our results suggest that suppression of superoxide production by a therapeutic dose of lidocaine correlates strongly with suppression of p47 phox translocation. IMPLICATIONS: We report on the effects of lidocaine on superoxide production in opsonized zymosan-activated neutrophils. Lidocaine suppresses superoxide production in a dose-dependent manner. This suppression correlates strongly with the suppression of translocation of p47 phox, a new subunit of NADPH-oxidase.

Adult↗
PubMed1990

The effect of local deep microwave hyperthermia on experimental zymosan-induced arthritis in rabbits.

The effect of local deep microwave hyperthermia (LDMWH) on normal and Zymosan-induced arthritis has been evaluated in 12 rabbits (24 joints). LDMWH, four treatments to each joint (twice weekly for a period of 2 wk), was generated by an antenna operating at 915 MHz for 60 min, reaching an intraarticular temperature of 42.5 +/- 0.5 degrees C. A surface cooling system was used with the microwave apparatus. Two weeks after the last treatment, all animals were sacrificed. The application of LDMWH on normal joints induced a limited proliferation of the synovial lining cells with a minimal perivascular infiltration of mononuclear and neutrophil cells. However, no histologic damage to the skin, muscles, bone, cartilage or bone marrow adjacent to the heated joints could be noted. Induction of Zymosan arthritis (2 wk before LDMWH) was characterized by pannus formation and granulomatous reaction accompanied by fibrinoid deposits and disseminated necrotic foci in the synovial intima. The LDMWH treatment on the examined arthritic joints brought about a reduction in the degree of granulomatous reaction concomitant with the appearance of some fibrocytes and fine collagen fibrils. These findings suggest that LDMWH can be safely applied, even repeatedly, without morphologic evidence of damage to any normal mesenchymal tissue. Moreover, it reduces the inflammatory process in experimentally induced synovitis.

Animals↗
PubMed1994

Comparison between lung and liver lipid peroxidation and mortality after zymosan peritonitis in the rat.

We compared the mortality rate and the lung and liver histologic injury with the degree of tissue lipid peroxidation after zymosan-induced peritonitis. Male Wistar rats were given .75 or 1 mg/g of zymosan intraperitoneally and monitored for 24 h. Tissue lipid peroxides were measured as conjugated dienes and malondialdehyde (MDA) as were the antioxidants, ascorbic acid and catalase. Mortality rates for the .75 and 1 mg/g groups were 15 and 50%, respectively. In lung, the degree of increase in conjugated dienes and MDA was significantly greater in nonsurvivors than survivors. Ascorbic acid and catalase levels were also significantly decreased to a greater degree in the sicker animals with ascorbic acid decreased to a greater degree in the higher dose and sicker animals. The level of MDA corresponded with the degree of histologic change. Catalase decreased to a greater degree in liver than lung. We conclude that the degree of lung and liver lipid peroxidation correlates with the degree of inflammation induced tissue injury and mortality.

Analysis of Variance↗
PubMed2005

Zymosan-induced generalized inflammation: experimental studies into mechanisms leading to multiple organ dysfunction syndrome.

Patients suffering from multiple organ dysfunction syndrome (MODS) comprise a heterogeneous population, which complicates research in its pathogenesis. Elucidation of the mechanisms involved in the development of MODS will ultimately necessitate the collection of tissue samples and the performance of invasive procedures. These requirements greatly reduce the possibilities for research in human subjects. Therefore, an animal model for MODS is a necessary and valuable tool. In the mid 1980s, the zymosan-induced generalized inflammation (ZIGI) model was introduced. Intraperitoneal injection of zymosan in mice or rats leads, in the course of 1 to 2 weeks, to increasing organ damage and dysfunction. The ZIGI model has been recognized as the one that best resembles human MODS and it has been used widely to study systemic inflammation in relation to organ failure. This review describes the ZIGI model and gives an overview of the results obtained.

Animals↗
PubMed1994

Leukotriene B4 and C4 generation by blood leukocytes after ex vivo stimulation by Ca-ionophore and opsonized zymosan in children with atopic dermatitis.

The ex vivo release of leukotrienes B4 (LTB4) and C4 (LTC4) from the leukocytes of children with atopic dermatitis (AD) was evaluated after stimulation with Ca-ionophore and opsonized zymosan and compared with that of control children of similar ages. The blood eosinophil counts and total serum IgE levels in AD children were significantly higher than those in control children. The production of LTC4, but not LTB4, was significantly higher in AD children than in control children. There was a significant correlation between the relative blood eosinophil count and LTC4 generation after stimulation with both Ca-ionophore and opsonized zymosan in all subjects. Calculations of the amount of LTC4 produced per eosinophilic cell showed that there was no significant difference between cells from AD children and control children in terms of their ability to produce LTC4. These findings suggest that the enhanced LTC4 generation is due to increased numbers of eosinophils rather than to enhanced releasability of these cells.

Adolescent↗
PubMed1981

Superoxide release by zymosan-stimulated rat Kupffer cells in vitro.

Kupffer cells were isolated from pronase-perfused rat livers and were maintained as a monolayer culture in a state of high purity and viability. Immediately after contact with zymosan particles, O2 uptake of the Kupffer cells increased fivefold; about 50% of the net oxygen consumed was accounted for as superoxide released into the medium. Concomitantly, a transient burst of luminol-dependent chemiluminescence, an increased activity of NAD(P)H oxidase and a stimulation of the flow of glucose through the hexose monophosphate shunt were observed. Chemiluminescence and O2- production were almost completely inhibited by superoxide dismutase and iodoacetate. Zymosan-induced chemiluminescence was not inhibited in the presence of the non-penetrating thiol reagents, 5,5'-dithio-bis-2-nitrobenzoate and iodoacetyl-sepharose. Iodoacetate acted on the cytosolic glucose-6-phosphate dehydrogenase rather than on NAD(P)H oxidase of the cell membrane.

Animals↗
PubMed1991

Role of granulocytes and C5a in myocardial response to zymosan-activated serum.

Although previous studies have demonstrated that complement (C)5a causes myocardial ischemia and mechanical dysfunction, the cardiac response of endogenously produced C5a and C5a des-Arg in zymosan-activated serum (ZAS) and the critical role of granulocytes in this process are poorly understood. Therefore, we compared the coronary and cardiac effects of ZAS and purified C5a and investigated the role of leukocyte adhesion-promoting receptors (i.e., CD11/CD18). Like purified C5a, ZAS (0.5 ml) significantly reduced coronary artery blood flow and regional segment shortening, whereas coronary venous granulocyte concentration and myocardial lactate extraction were significantly decreased. A monoclonal antibody (MoAb) to C5a/C5a des-Arg attenuated ZAS-induced cardiac alterations. Three minutes of continuous infusion of C5a or ZAS induced sustained decreases in coronary venous granulocyte concentrations, although coronary flow and segment shortening returned to control levels after 2 min. Another MoAb, IB4, directed against CD18, significantly inhibited ZAS-induced granulocyte extraction and associated cardiac effects. Thus, cardiac dysfunction occurs after activation of the complement cascade with zymosan resulting in extraction of granulocytes mediated by the CD18 adherence glycoprotein. Furthermore, intramyocardial retention of granulocytes appears necessary for the initial and full ZAS-induced cardiac dysfunction.

Anaphylatoxins↗
PubMedDate not supplied

Thermal response to zymosan: the differential role of complement.

OBJECTIVES: This study was designed to determine whether the complement (C) system may be involved in the febrile response to zymosan (Zym), a glycan derived from yeast cell walls. METHODS: Cobra venom factor (CVF) at 100 U/animal or its vehicle, pyrogen-free saline (PFS), was injected intravenously (i.v.) into guinea pigs to deplete serum C. Eighteen hours later, a low or high dose of Zym or its vehicle, PFS, was administered i.v. or intraperitoneally (i.p.) to these animals. The core temperature (T(c)) was measured continuously by thermocouples. Serum C levels were determined by sheep erythrocyte hemolytic assay. RESULTS: Zym at 1 mg/kg caused a 1 degrees C T(c) rise that was not significantly affected by CVF pretreatment. However, CVF-induced hypocomplementation converted the T(c) fall ( approximately 1.2 degrees C) produced by 100 mg/kg of Zym i.p. into a 1 degrees C T(c) rise. Similarly, CVF pretreatment did not affect the T(c) rise caused by 0.5 mg/kg of Zym i.v., but converted the T(c) fall induced by 25 mg/kg i.v. into a 1 degrees C T(c) rise. A separate experiment showed that 25, but not 0.5 mg/kg of Zym i.v., decreased serum C by 34% in 15 min; C did not recover over the next 6 h. A second i.v. injection of 25 mg Zym/kg 210 min later, when the T(c) had recovered but the serum C had not, yielded a smaller and briefer T(c) fall. CONCLUSION: These results suggest that Zym is inherently pyrogenic, but this effect is manifested only when the dose of zymosan is too small to activate C or when C has been reduced by prior activation.

Animals↗
PubMed1994

Eosinophil chemiluminescence response to cytokines and opsonized zymosans in atopic dermatitis.

Chemiluminescence (CL) responsiveness of eosinophils (Eos) to zymosan particles coated with either IgG, C3 or both and eosinophilopoiesis-modulating cytokines was investigated in patients with atopic dermatitis (AD), and an attempt was made to correlate these CL responses with serum levels of eosinophil cationic protein (ECP) which increased in response to the extent of AD severity, but not blood eosinophil counts. A high degree of positive correlation existed between serum levels of ECP and either IgG containing opsonized zymosan- or interleukin-5 (IL-5)-induced CLs. The CL values induced by these two stimuli appeared to be directly correlated with the intensity of each ligand-linked receptor expression. These results suggested that Fc gamma RII-and/or IL-5R-mediated eosinophil activation at the site of lesional skins might implicate in deterioration of cutaneous inflammation, and consequently cause an elevation of serum levels of ECP in AD.

Blood Proteins↗
PubMed1991

Effects of zymosan-activated human granulocytes on isolated human airways.

In asthma a temporal association exists between the late allergic reaction (LAR), the influx of granulocytes into the airway wall, and an increase in bronchial responsiveness. We therefore tested the hypothesis that activated human granulocytes constrict isolated human airways and increase their sensitivity to cholinergic stimuli. Bronchial rings were dissected from 23 lung tissue specimens collected at thoracotomy and studied isotonically in organ baths. Airways were incubated with 1, 2, 5, 10, or 20 x 10(6) granulocytes from normal or atopic donors. Activation of the cells with serum-treated zymosan (STZ, 0.2 mg/ml), which itself did not alter baseline airway caliber, resulted in a bronchoconstriction proportional to the number of zymosan-activated granulocytes (ZAG) present (rs = 0.79, p less than 0.001). This contraction was reduced by about 70% with the leukotriene C4/D4 receptor antagonist FPL 55712 (11.5 microM; p less than 0.001) or with the lipoxygenase inhibitor nordihydroguaiaretic acid (10 microM; p less than 0.001). The scavengers of activated oxygen molecules superoxide dismutase (300 U/ml) and bovine catalase (5,000 U/ml), the cyclooxygenase inhibitor indomethacin (10 microM), or the histamine (H1) receptor antagonist mepyramine (2.8 microM) had no effect. Granulocyte suspensions from atopic donors contained more eosinophils (p less than 0.001), and the magnitude of the contraction to 10 x 10(6) ZAG was related to the proportion of eosinophils (rs = 0.66, p less than 0.01). The sensitivity of the airways to methacholine was unchanged in the presence of 1, 2, or 5 x 10(6) ZAG and decreased with 10 or 20 x 10(6) ZAG (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗