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PubMed1992

Effects of nerve stimulation and zymosan on glycogenolysis in perfused livers from cold-exposed rats.

The effects of sympathetic nerve stimulation and zymosan (cell wall particles from yeast) on glycogenolysis were studied in perfused livers from rats kept for 5 and 20 days at 4 degrees C. The rate of glycogenolysis induced by nerve stimulation decreased significantly without any decrease in norepinephrine outflow during cold exposure, and the rate induced by norepinephrine did not change. By contrast, the rate of zymosan-induced glycogenolysis increased markedly during cold exposure. The rats with denervated hepatic nerves did not show the increased response to zymosan. In cold-exposed rats, both mepacrine and ibuprofen inhibited the effects of zymosan and of nerve stimulation without any inhibition of the outflow of norepinephrine. Neither inhibitor had any effect on the effects of norepinephrine. The metabolic effects of nerve stimulation and zymosan were not additive in cold-exposed rats. These results suggest that cold exposure may modulate the metabolism of arachidonic acid in Kupffer cells via hepatic nerve and decrease the eicosanoid-dependent glycogenolysis by nerve stimulation.

Animals↗
PubMed1998

Aggravating action of zymosan on acute liver damage in perfused liver of rats treated with D-galactosamine.

To study the role of Kupffer cells in the aggravation of liver injury, effects of zymosan on acute liver damage were explored using perfused livers of rats 24 h after intraperitoneal injection of D-galactosamine (800 mg/kg). The leakage of lactate dehydrogenase and aspartate aminotransferase into the effluent was used to indicate acute liver damage. Infusion of zymosan (30 microgram/ml) into the portal vein rapidly increased the leakage of lactate dehydrogenase and aspartate aminotransferase from galactosamine-treated liver with decreased perfusion flow. Pretreatment of animals with gadolinium, which diminished an immunostaining of resident macrophages in the injured liver, significantly attenuated the flow reduction induced by zymosan, whereas it did not affect the increases in enzyme leakage. Infusions of PGF2alpha, PGE2, and leukotriene D4, the eicosanoids mainly produced by Kupffer cells, decreased perfusion flow without rapid augmentation of enzyme leakage from galactosamine-treated liver. These results indicate that zymosan potentiates acute liver damage after galactosamine injection and suggest that certain types of nonparenchymal cells other than Kupffer cells are mainly involved in the action of zymosan.

Acute Disease↗
PubMed1997

Physiological and cytokine responses in IL-1 beta-deficient mice after zymosan-induced inflammation.

Interleukin (IL)-1 beta-deficient (IL-1 beta -/-) mice exhibited decreased zymosan-induced lethality and reduced production of IL-6 compared with wild-type controls (IL-1 beta +/+). In addition, IL-1 beta -/- mice had a diminished cellular infiltrate (33%) in the peritoneal cavity after zymosan. However, anorexia and hypoglycemia were not affected by the lack of IL-1 beta. The induction of corticosterone was only slightly reduced (14%) in IL-1 beta -/- mice. Peritoneal lavage fluid levels for IL-1 alpha, but not for tumor necrosis factor (TNF)-alpha, were also decreased. To evaluate the role of residual IL-1 alpha production in IL-1 beta -/- mice, we used IL-1-receptor antagonist (IL-1ra). In IL-1 beta +/+ mice, IL-1ra inhibited production of IL-6 after zymosan, without affecting TNF-alpha synthesis. There was no further inhibitory effect of IL-1ra on IL-6 production in IL-1 beta -/- mice, suggesting no role for IL-1 alpha in zymosan-induced IL-6. Our results demonstrate that IL-1 beta plays a significant, although not exclusive, role in the physiological and cytokine responses to zymosan-mediated inflammation.

Analysis of Variance↗
PubMed1995

Involvement of leukotriene B4 in zymosan-induced rat pleurisy: inhibition of leukocyte infiltration by the 5-lipoxygenase inhibitor T-0757.

The role of leukotriene B4 (LTB4) in leukocyte infiltration in zymosan-induced rat pleurisy was investigated by studying the effects of 5-lipoxygenase inhibitors, T-0757 and AA-861, and a cyclooxygenase inhibitor, indomethacin, on leukocyte infiltration and LTB4 levels in the inflammatory exudate of rat pleurisy induced by intrapleural injection of zymosan (20 mg/rat). T-0757 and AA-861 inhibited the infiltration of leukocytes, mainly neutrophils, 3 h after injection of zymosan at a dose of 100 mg/kg, p.o., but indomethacin did not do so at a dose of 5 mg/kg, p.o. LTB4 was detected in the exudate 1 h after zymosan injection, and its level peaked at 3 h (45.4 +/- 8.6 ng/rat) and decreased thereafter. These LTB4 levels were depressed by T-0757 and AA-861 in a dose-dependent manner. T-0757 completely prevented LTB4 production at a dose of 100 mg/kg. These observations suggest that the inhibition of leukocyte infiltration is mediated by the inhibition of LTB4 production, and that LTB4 is one of the main chemical mediators of leukocyte infiltration in zymosan-induced rat pleurisy.

Amides↗
PubMed2000

Zymosan phagocytosis by mouse peritoneal macrophages is increased by apoHDL- and not by intact HDL-covered particles.

The uptake of lipids and lipoprotein particles by macrophages undergoes phagocytic activation and the formation of foam cells are key events in atherosclerosis. In this study we determined how intact high density lipoproteins (HDL) and apolipoproteins-HDL (removal of the lipid component from HDL, i.e., apoHDL) influence the phagocytosis of zymosan by mouse peritoneal macrophages. Zymosan particles preincubated together with lipoproteins or alone (control) were incubated with the macrophages. Phagocytosis activity was reported as the percent of macrophages that internalized three or more zymosan particles. HDL co-incubated with zymosan did not influence the over-all uptake of zymosan particles compared to apoHDL, which greatly enhanced the ability of the particle to be phagocytized (P<0.001). Part of this effect might be related to a greater binding of apoHDL to the particles compared to that of HDL (P<0.05). We conclude that this can be a useful method to study the ability of lipoproteins, including modified lipoproteins obtained from subjects with genetic forms of hyperlipidemia, to opsonize particles such as red blood cells and thus to investigate the processes that control the formation of foam cells and the mechanisms of atherogenesis.

Animals↗
PubMed1999

Acidification of the phagosome in Crassostrea virginica hemocytes following engulfment of zymosan.

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.

Animals↗
PubMed2000

Carbohydrate-carbohydrate interaction: zymosan and beta-glucan from Saccharomyces cerevisiae bind mannosylated glycoconjugates.

Zymosan from cell wall of the yeast Saccharomyces cerevisiae was found to interact with synthetic and natural glycoconjugates; mannose-rich glycoprotein N-chains demonstrated the maximal affinity. The carbohydrate-carbohydrate nature of the interaction has been confirmed by the following data: 1) periodate treatment of the zymosan impairs the binding; 2) neither protease nor alkali treatment of the zymosan weaken the binding; 3) beta-glucan from S. cerevisiae, which is the major zymosan component, interacts with glycoconjugates similarly to zymosan. The binding is reversible, Ca2+-dependent, and cooperative; it can be dose-dependently inhibited by saccharides relative to one of the partners of the carbohydrate-carbohydrate interaction.

Calcium↗
PubMed2003

[A small dose of intraperitoneal injection of zymosan induces systemic inflammatory response and multiple organ dysfunction following gut ischemia-reperfusion injury].

OBJECTIVE: To investigate the effects of a small dose of intraperitoneal injection of zymosan following gut ischemia-reperfusion injury on systemic inflammatory response and distant organ function. METHODS: Wistar rats were randomly divided into three groups: gut ischemia-reperfusion injury (I-R) alone, intraperitoneal injection of zymosan (Z) alone, and gut ischemia-reperfusion followed by intraperitoneal injection of zymosan (M). Gut (I-R) was produced by occluding superior mesenteric artery for 60 minutes followed by gut reperfusion. A small dose(125 mg/kg) of zymosan was given intraperitoneally at 12 hours after recovery of gut blood flow. RESULTS: Systemic inflammatory responses were found in all rats of three groups. The plasma level of tumor necrosis factor-alpha and activities of myeloperoxidase in lungs and intestines were significantly higher in animals in M group compared with those in I-R and Z groups. The incidence of multiple organ dysfunction syndrome (MODS) and mortality rate at 72 hours postinjury in two-hits group were significantly higher than those in I-R and Z group. CONCLUSION: A small dose of intraperitoneal injection of zymosan could induce systemic inflammatory response and multiple organ dysfunction more readily when there is a precedent gut ischemia-reperfusion injury.

Animals↗
PubMed1978

Zymosan-induced resistance to endotoxin and hemorrhagic shock.

Improved surgical techniques and judicial use of available antibiotics have reduced the number of postoperative complications over the past decade. However, septic and hemorrhagic shock occur all too frequently, and each carries with it an appreciable morbidity and mortality. Endotoxins and hemorrhage are both known to suppress the phagocytic activity of the reticuloendothelial system (RES). On the other hand, zymosan, a yeast (Saccharomyces cerevisiae) cell wall preparation administered intravenously, results in temporary RES hyperplasia and increased phagocytic activity. Dogs were pretreated with zymosan to determine the degree of RES stimulation and protection against endotoxin and hemorrhagic shock attainable. Twenty-five dogs received intravenous zymosan (10 mg/kg) on days 1, 2, and 3. Another 24 dogs served as controls. On day four, one-half the animals in each group received E coli endotoxin (1.5 mg/kg) intravenously. The other animals underwent two hours of hemorrhagic shock at a mean blood pressure of 40 mm Hg. Seventy-two hour survival was as follows: Endotoxin treated, 66.7% (8/12); endotoxin control, 27% (3/11); hemorrhagic treated, 53.3% (8/15); and hemorrhagic control, 28.6% (4/14). Hemodynamic, metabolic, and lysosomal enzyme parameters were evaluated. No zymosan toxicity was observed. These findings suggest that an RES stimulant such as zymosan could be incorporated as preoperative adjunctive therapy to induce resistance to these shock syndromes in the elective surgical patient.

Animals↗
PubMed1988

Phagocytosis of serum-opsonized zymosan down-regulates the expression of CR3 and FcRI in the membrane of human monocytes.

The effect of iC3b receptor (CR3)-mediated phagocytosis on the expression of CR (C3b receptor, CR3) and IgG FcR (FcRI, FcRII) has been investigated by using serum-opsonized zymosan as a multivalent ligand for CR3. Sixteen hours after a short (1-h) pretreatment of human monocyte monolayers with zymosan opsonized with human AB serum (250 micrograms/ml), CR3 expression (as assessed by flow cytometric analysis with mAb Mo1) was significantly reduced by 59 +/- 3% (mean +/- SEM, n = 15, p less than 0.001). Concomitant with CR3 down modulation, FcR binding activity (as assessed by binding of IgG-coated E) was also found to be decreased to 41 +/- 4% of control (n = 7, p less than 0.001). Reduced FcR function was paralleled by a decrease in the expression of FcRI (as assessed with mAb 32.2). This FcRI modulation was not caused by zymosan-bound IgG because zymosan opsonized with agammaglobulinemic serum equally down regulated CR3 and FcRI expression. Pretreatment with zymosan opsonized with human AB serum, however, did not change the expression of other IgG and C-binding sites such as FcRII (examined with mAb IV.3 and 2E1) and CR1 (assessed with mAb 57F) as well as of unrelated cell membrane structures (beta 2m, MHC class II). In contrast, co-modulation for FcR function and CR3 expression induced by polymeric IgG is accompanied by a decreased expression of FcRII. These data indicate that interaction of a specific receptor with its ligand not only changes the expression of the receptor triggered, but has also a modulating effect on other receptor systems on the same cell.

Antigens, Differentiation↗
PubMed1986

The role of opsonins in vacuolar sealing and the ingestion of zymosan by human neutrophils.

After opsonization with whole human serum, with IgG antibody alone or with C3 fragments alone, the ingestion of zymosan particles by human neutrophils was found to correlate most closely with the efficiency of C3 fragment deposition on the zymosan surface. Selective opsonization of zymosan particles with IgG did not promote phagocytosis at all in suspension, but could promote ingestion after particle-cell contact was induced by centrifugation. In contrast, zymosan particles in suspension selectively opsonized by C3 fragments were ingested as efficiently as those opsonized with whole serum, and we suggest that C3 fragments provide the principal stimulus for phagocytosis of zymosan. The process of vacuolar sealing was not dependent on the state of opsonization of the particles and was significantly more efficient with unopsonized particles, indicating that formation of unsealed vacuoles is not due to a failure of the 'zipper' mechanism of sequential interaction of cell surface receptors and opsonic ligands.

Adult↗
PubMed1981

Opsonized zymosan-stimulated granulocytes-activation and activity of the superoxide-generating system and membrane potential changes.

Phagocytic cells generate superoxide in response to stimulation by opsonized particles. A continuous assay for opsonized zymosan-stimulated granulocyte superoxide production shows that there is a lag time between the addition of particles and the onset of detectable superoxide production. Superoxide production is preceded by membrane potential depolarization. Neither superoxide production nor membrane depolarization occurs in granulocytes from patients with chronic granulomatous disease. The extent of activation by opsonized zymosan is affected by the dose of zymosan from 0.5 to 4.5 mg/ml, but the time necessary for activation (lag time) is not. Similarly, the extent of depolarization but not the time necessary for attaining maximum depolarization is concentration-dependent. Effects of temperature, divalent cations, 2-deoxyglucose, cyanide, and N-ethyl maleimide on superoxide production are similar for granulocytes treated with soluble stimuli and with opsonized zymosan. Thus, zymosan stimulates granulocytes to generate superoxide and undergo membrane depolarization in a manner similar to that elected by soluble stimuli.

Animals↗
PubMed1981

Circadian fluctuations in the activity of phagocytic cells in blood, spleen, and peritoneal cavity of mice as measured by zymosan-induced chemiluminescence.

Circadian variations in the phagocytic activity of mouse whole blood, spleen, and peritoneal cells were studied using the zymosan-induced chemiluminescence assay as a measure of phagocytosis. On a regimen providing for light from 7:00 to 19:00 alternating with darkness, the phagocytic activity of mouse blood, spleen, and peritoneal cells was high around 10:00 and low around 22:00, the integrated counts of chemiluminescence being 82.33 x 10(5) and 52.76 x 10(5) for peritoneal cells, 83.3 x 10(5) and 32.2 x 10(5) for spleen cells, and 12.33 x 10(5) and 3.99 x 10(5) for blood cells. Variations of a similar tendency were also found in blood leukocyte and granulocyte counts, the counts being again higher at 10:00 compared with the blood samples withdrawn at 22:00. In contrast to the differences in the intensity of the zymosan-induced chemiluminescence, the shapes of the curves (Fig. 6) of each cell preparation were similar, irrespective of the time period of the day the cells were prepared. Comparison of the zymosan-induced chemiluminescence curves of the 3 cell suspensions studied, prepared at the same period of the day, revealed some similarity between the kinetics of blood and spleen samples; the intensity, however, of zymosan-induced chemiluminescence emitted by spleen cells was much higher. The kinetics of zymosan-induced chemiluminescence curves of peritoneal cells differed from the other 2, being slower at the onset, the chemiluminescence lasting for a longer time and declining more slowly. We have shown here circadian variations in the activity of mouse phagocytic cells. The simple and rapid method of chemiluminescence measurements used in this study appears to be a powerful tool for the further investigation of such circadian variations.

Animals↗
PubMed1980

Enhanced vascular permeability and haemorrhage-inducing activity of zymosan-activated plasma.

The intradermal injection into rabbits of various phagocytosible materials is known to induce polymorphonuclear leucocyte infiltration, protein exudation and microvascular haemorrhage. The injection of rabbit plasma, in which complement is activated with zymosan, also induces polymorphonuclear leucocyte infiltration. We investigated the effect of this soluble, non-ingestible stimulus to polymorphonuclear leucocyte accumulation on vascular integrity. Vascular permeability, measured with 125I-human serum albumin, was markedly but only transiently increased 1 hr after zymosan-activated plasma injection. In contrast, haemorrhage or red blood cell extravasation, measured with 59Fe-labelled red cells, developed only 4 hr after zymosan-activated plasma injection and continued for at least 10 hr. A direct correlation was found between the number of infiltrating polymorphonuclear leucocytes as measured with 51Cr-labelled leucocytes, and the degree of haemorrhage. Histological sections confirmed these changes. Plasma that was heat-inactivated (56 degrees C, 30 min) or made functionally C5-deficient prior to zymosan activation, failed to induce haemorrhage and caused no, or only mild , leucocyte infiltration. It is postulated that the C5ades arg in zymosan-activated plasma not only induces polymorphonuclear leucocyte infiltration but also, directly or indirectly, causes microvascular damage.

Animals↗
PubMedDate not supplied

Presence of immunoreactive platelet-activating factor in peritoneal exudate induced by zymosan in rats.

The presence of the platelet-activating factor (PAF) in peritoneal exudate, induced by zymosan, was investigated in rats. Intraperitoneal injection of zymosan induced an extravasation of plasma proteins and an accumulation of polymorphonuclear leukocytes in the peritoneal cavity. Zymosan induced a release of immunoreactive PAF in peritoneal exudate which reached maximum levels at 30 min and then declined slowly. Immunoreactive PAF was evenly distributed in the fluid and cellular fractions of the exudate. A PAF-acetyltransferase activity was found as well in the exudate as in plasma. Histamine levels, measured by bioassay, increased after injection of zymosan, reached a peak at 15 min and declined to a normal level within 4 hr. Protein extravasation was inhibited by WEB 2086, a PAF antagonist, during the 6 hours of the study, whereas the accumulation of leukocytes was suppressed at 2 hour by WEB 2086 and SM 12502, two PAF antagonists. PAF is present in the peritoneal exudate induced by zymosan in rats, and plays a role in the development of the inflammatory response. Its main origin might be resident macrophages and polymorphonuclear leukocytes.

Acetyltransferases↗
PubMed1997

Intraplantar zymosan as a reliable, quantifiable model of thermal and mechanical hyperalgesia in the rat.

The study of the mechanisms of thermal and mechanical hyperalgesia produced in human inflammatory conditions is dependent on a reliable, consistent model. The present investigation shows that the intraplantar administration of zymosan in the rat hindpaw produces a reliable and quantifiable thermal and mechanical hyperalgesia accompanied by oedema that closely mimics the symptoms of inflammation in man. Prior to the intraplantar injection of zymosan, there was no significant difference in withdrawal latencies, mechanical withdrawal thresholds or paw thickness between the left and right hindpaws. The intraplantar injection of zymosan (0.313-6.25 mg), an extract from yeast, produced a dose- and time-dependent thermal and mechanical hyperalgesia, a robust oedema and, at the greatest doses, produced evidence of spontaneous pain. At the least dose of zymosan tested (0.313 mg), there was a slight oedema; oedema was greatest at dosages > or =2.5 mg and was always maximal by 30 min postinjection, irrespective of the dose. On the other hand, thermal and mechanical hyperalgesia showed a more complex dose- and time-dependence. Mechanical hyperalgesia did not appear until dosages > or =1.25 mg and was maximal by 5 mg. In addition, mechanical hyperalgesia showed a time-dependent progressive onset so that hyperalgesia was maximal by the 4-h testing time-point. In contrast, thermal hyperalgesia showed a biphasic nature with two apparent maximal time-points (30 min and 4 h). There was an early-phase thermal hyperalgesia (maximal by 30 min) that was dose-dependent at dosages > or =2.5 mg (not apparent at lower dosages) and a late-phase (maximal by 4 h) that was dose-dependent at dosages > or =0.0625 mg. At the greatest doses administered (5 and 6.25 mg), there was evidence of spontaneous pain from the time of injection for up to 4 h that was characterized by occasional spontaneous flicking of the hindpaw, but more usually by holding the paw in an elevated position for extended periods of time. In addition, at the greatest dose tested (6.25 mg), all rats showed evidence of licking, biting and shaking of the injected hindpaw for up to 30-45 min after injection. These data demonstrate that the intraplantar injection of zymosan is a reliable and quantifiable model of tonic pain characterized by a dose- and time-dependent thermal and mechanical hyperalgesia accompanied by a robust oedema. This model is likely to be a useful, reliable model in which to study further the central and peripheral mechanisms of hyperalgesia.

Journal Article↗
PubMed1980

The in vitro immune response in the absence of serum and its proteins: stimulating activity of zymosan.

In the absence of serum and its components, zymosan, together with 2-mercaptoethanol present in the medium, stimulated the in vitro primary immune response. Zymosan was effective at a concentration of as low as 2.5 microgram/ml. Removal of macrophages using iron powder resulted in higher recoveries of plaque-forming cells in the presence of zymosan but not of fetuin. Since insoluble zymosan may be easily removed from the culture, the test system described might be suitable for the identification of specific control factors secreted by cells during the in vitro immune response.

Animals↗
PubMed1992

Protein kinase C involved in zymosan-induced release of arachidonic acid and superoxide but not in calcium ionophore-elicited arachidonic acid release or formation of prostaglandin E2 from added arachidonate.

Zymosan and phorbol ester induced in liver macrophages the release of arachidonic acid, prostaglandin E2, and superoxide; the calcium ionophore A 23187 elicited a release of arachidonic acid and prostaglandin E2 but not of superoxide, and exogenously added arachidonic acid led to the formation of prostaglandin E2 only. The zymosan- and phorbol-ester-induced release of arachidonic acid, prostaglandin E2, and superoxide was dose-dependently inhibited by staurosporine and K252a, two inhibitors of protein kinase C, and by pretreatment of the cells with phorbol ester which desensitized protein kinase C. The release of arachidonic acid or prostaglandin E2 following the addition of A 23187 or arachidonic acid was not affected by these treatments. Zymosan and phorbol ester but not A 23187 or arachidonic acid induced a translocation of protein kinase C from the cytosol to membranes in intact cells. These results demonstrate an involvement of protein kinase C in the zymosan- and phorbol-ester-induced release of arachidonic acid, prostaglandin E2, and superoxide; the release of arachidonic acid and prostaglandin E2 elicited by A 23187 and the formation of prostaglandin E2 from exogenously added arachidonic acid, however, is independent of an activation of protein kinase C.

Alkaloids↗