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PubMed1986

Inhibitory effects of a novel synthetic protease inhibitor, FUT-175, on the paw edema in rats and zymosan-induced complement activation in vitro.

FUT-175 inhibited the zymosan-induced rat paw edema in a dose-dependent manner, while indomethacin exhibited no significant activities in this model. FUT-175 also inhibited the decrease in hemolytic complement (CH50) induced by zymosan in vitro, and indomethacin was inactive. These results suggest that FUT-175 has potent in vitro and in vivo inhibitory activity against the activation of the complement system induced by zymosan.

Animals↗
PubMed1983

Suppression of zymosan-induced chemiluminescence of whole blood by conjugates composed of drug, guinea pig skin extracts and sera from patients with suspicious drug eruptions.

Conjugates composed of drug, guinea pig skin soluble fraction, and sera from 50 patients with various types of drug eruptions were prepared by the incubation of these mixtures for 60 min at 37 degrees C. And the effects of conjugates on zymosan-induced chemiluminescence (ZI-CL) in whole blood were examined. The conjugates obtained from 32 cases significantly suppressed ZI-CL of whole blood. The mean value of peak intensities of CL in the presence of their conjugates showed 62% of those after the pretreatment of mixtures consisting of drug, soluble fraction and sera from healthy donors. In the systems of non-opsonized and opsonized zymosan-induced CL of leukocyte-erythrocyte sediment, similar inhibitory effects were obtained in both systems in the presence of conjugates, but the time course of CL response was slower in the system with non-opsonized zymosan. In other experiments with the use of immune complexes, which were formed by human albumin and antihuman albumin goat serum in vitro, soluble immune complexes suppressed ZI-Cl of whole blood. These results suggest that immune complexes may be formed during incubation of conjugates and block the receptors on the surfaces of granulocytes, resulting in the suppression of ZI-CL.

Animals↗
PubMed1998

Nitric oxide production in human macrophagic cells phagocytizing opsonized zymosan: direct characterization by measurement of the luminol dependent chemiluminescence.

When differentiated into mature macrophages by the combination of all-trans retinoic acid and 1,25-dihydroxyvitamin D3, the human promonocytic cell lines U937 and THP-1 expressed inducible nitric oxide synthase (iNOS) transcripts. During their differentiation, the cells acquired the capacity to produce not only superoxide anion (O2.-) but also nitric oxide (.NO) in response to IgG (or IgE)-opsonized zymosan. The inhibitors of the iNOS pathway, aminoguanidine and NG-monomethyl-L-arginine (L-NMMA), suppressed the production of .NO and enhanced the steady-state concentration of O2.- determined. Conversely, superoxide dismutase (SOD) scavenged the O2.- released and increased the .NO-derived nitrite concentration detected. These data suggested a possible interaction between O2.- and .NO. In differentiated U937 (or THP-1) cells, IgG or IgE-opsonized zymosan induced a strong time-dependent luminol-dependent chemiluminescence (LDCL), which was abrogated by SOD and partially inhibited by aminoguanidine or L-NMMA. Since the iNOS inhibitors did not directly scavenge O2.-, LDCL determination in the presence or absence of SOD and/or iNOS inhibitors demonstrated a concomitant production of O2.- and .NO. These radicals induced the formation of a .NO-derived product(s), probably peroxynitrite (ONOO-), which was required to elicit maximal LDCL. Finally, LDCL measurement provided a convenient tool to characterize iNOS triggering and demonstrated an interaction between NADPH oxidase and iNOS products in human macrophagic cells phagocytizing opsonized-zymosan. These findings show that in activated macrophages, iNOS activity can be involved in LDCL and support the debated hypothesis of iNOS participation to the microbicidal activity of human macrophages.

Calcitriol↗
PubMed2002

Cyanidin 3-O-beta-D-glucoside suppresses nitric oxide production during a zymosan treatment in rats.

Anthocyanins are used for food color, and they are widely distributed in the human diets, suggesting that we ingest considerable amounts of anthocyanins from plant-based daily diets. We have demonstrated that a typical anthocyanin, cyanidin 3-O-beta-D-glucoside (C3G), suppressed the zymosan-induced inflammatory response in rats when it was orally administered. The elevation of the peritoneal exudate NOx, tumor necrosis factor (TNF) alpha interleukin-1beta (IL-1beta), IL-6, and the cytokine-induced neutrophil chemoattractant-1 (CINC-1) concentrations were significantly suppressed by the administration of C3G. The zymosan treatment resulted in an increase in the serum alpha2-macroglobulin and decreases in the serum albumin and transferrin levels, which are recognized as acute phase proteins. However, these levels were normalized by the administration of C3G. The inducible nitric oxide synthase (iNOS) protein level in the peritoneal exudate cells was markedly elevated in the control group treated with zymosan. However, the administration of C3G significantly reduced the level of iNOS in the peritoneal exudate cells. Taken altogether, our findings provide a biochemical basis for the use of C3G as a functional food factor and can also have important implications for the prevention of the NO-mediated inflammatory diseases.

Acute-Phase Proteins↗
PubMed1976

Activation of the complement attack mechanism in the fluid phase and its control by C567-INH: lysis of normal erythrocytes initiated by zymosan, endotoxin, and immune complexes.

Addition of zymosan-serum complexes to guinea pig erythrocytes in guinea pig complement-EDTA was found to result in substantial lysis of the bystander cells in the presence of polycations such as poly-L-lysine of 178,000 daltons. Involvement of the alternative C pathway was shown, and the optimum time, temperature, and eruthrocyte and polycation concentrations were defined; a surprising efficiency was observed at low temperature and high cell concentrations. Several lines of evidence indicated that this hemolysis was mediated via the C567 complex of the C system and modulated by serum inhibitors of C567 (C567-INH): lysis was observed only with zymosan-serum complexes possessing C-consuming activity; it was not observed in C5-depleted guinea pig serum but was restored upon addition of purified C5; the addition of partially purified C567-INH insubstantially depressed hemolysis; and poly-L-lysine which is known to neutralize C567-INH in solution resulted in substantial enhancement of hemolysis. We also sought to determine whether the addition of complement activators directly to erythrocyte-serum mixtures could result in the hemolysis of bystander erythrocytes. It was found that zymosan, endotoxin, antigen-antibody complexes, and aggregated human gamma-globulin each could initiate such bystander lysis under appropriate conditions. Lysis again was favored by increased erythrocyte concentrations, low temperatures, and the presence of polycations such as poly-L-lysine, and was found to be mediated via the C system. C567-INH blocked cytolysis whereas poly-L-lysine potentiated hemolysis by neutralization of C567-INH. These experiments emphasize the propensity for C567 formation and lysis of bystander erythrocytes during C activation generally, the role of C567-INH in the control of this lysis, and the susceptibility of these interactions to modulation by highly charged macromolecules.

Animals↗
PubMed1992

Liver and serum lysosomal enzymes activity during zymosan-induced inflammation in mice.

Liver and serum lysosomal enzymes (acid glucosidases and cysteine proteinases) during zymosan-induced stimulation of MPS or MPR depression induced by GdCl3 have been studied. Zymosan was used as a model for study of inflammation in vivo. The development of inflammation induced by zymosan was followed by increase activity of macrophage activation markers - beta-N-acetylglucosaminidase (NAGlu) and beta-N-acetylgalactosaminidase (NAGal) in liver and serum. There was enhance of liver cysteine proteinases activity. Similar, less prominent (partly) data were obtained during macrophage depression induced by GdCl3.

Acid Phosphatase↗
PubMed2005

[Relationship between glomerular lesion and NF-kappaB p65 activity in rat multiple organ failure caused by zymosan].

AIM: To observe the relationship between NF-kappaB p65 activity and glomerular lesion in rat multiple organ failure (MOF) caused by zymosan. METHODS: Twenty female Wistar rats aged 6-8 weeks were divided randomly into two groups, ten each group. 24 hours after MOF model was induced successfully by intraperitoneal injection of zymosan-paraffin oil suspension, the rats were sacrificed and the functions of liver and kidney as well as blood gas were analysed. At the meaning time, the pathological change in renal tissues was examined by H.E, PAS, PASM and Masson staining, whereas the NF-kappaB p65 activity in glomeruli was detected by immunohistochemical staining and ELISA. RESULTS: The levels of PO(2) and pH in blood of MOF model group were significantly lower than those of control group, while the levels of serum ALT and Cr were quite to the contrary. Pathological examination showed that in MOF model rats, there were notable proliferation of glomeruli, partial sclerotic glomeruli and a large number of infiltrating inflammatory cells in glomeruli and periglomeruli. Besides, the activity of NF-kappaB p65 in rat glomeruli of MOF model group was significantly higher than that of control group(P<0.01), and the increased activity of NF-kappaB p65 was positively corelated to the cell number in glomeruli, and area density of basement membrane as well as mesangial area, but negatively correlated to the area density of capillary loop. CONCLUSION: The increase in the activity of NF-kappaB p65 may play an important role in glomerular lesions of MOF model rats caused by zymosan.

Animals↗
PubMedDate not supplied

Inhibition by WEB 2086, a PAG-acether antagonist of oedema and peritonitis induced by zymosan in rats.

WEB 2086 reduced the increase in vascular permeability induced by platelet-activating factor (PAF-acether) in rat abdominal skin. Injected alone, WEB 2086 did not modify the oedema induced by zymosan in rat paw. However, administered with methysergide and mepyramine, WEB 2086 reduced the development of this oedema during the first two hours. WEB 2086 also reduced the volume of the exudate induced by zymosan in the peritoneal cavity and its content in leucocytes. Methysergide and mepyramine reduced the volume of the peritoneal exudate. BW755C inhibited the peritoneal accumulation of fluid and of leucocytes. Indomethacin was inactive. The inhibitory effect of WEB 2086 suggests that PAF-acether is involved in the inflammatory responses induced by zymosan in rats beside other endogenous factors such as lipoxygenase products and mast cell amines.

4,5-Dihydro-1-(3-(trifluoromethyl)phenyl)-1H-pyraz↗
PubMed1990

Differential augmentation by recombinant human tumor necrosis factor-alpha of neutrophil responses to particulate zymosan and glucan.

Zymosan (Z) and its major insoluble carbohydrate component beta-linked glucan activate human neutrophils (PMN) through a trypsin-sensitive recognition mechanism. This mechanism is believed to involve the PMN CR3R. Both Z and glucan generated dose and time-dependent release of the secondary lysosomal granule marker vitamin B12 binding protein, leukotriene B4 (LTB4) and superoxide from PMN and were phagocytosed with similar dose-dependent kinetics. The PMN superoxide and LTB4 responses to glucan; however, were consistently greater than those to the same doses of Z. The phagocytosis of both particles was significantly reduced after partial digestion with beta-laminarinase but not beta-glucosidase or alpha-mannosidase suggesting a recognition mechanism dependent on intact beta-1,3-glucosidic bonds in both particles. TNF-alpha (rhTNF-alpha) promoted a time- and dose-dependent increase in the expression of PMN CR3 up to 60 min. The increased expression of CR3 was paralleled by the release of the secondary lysosomal granule marker vitamin B12-binding protein. This granule contains a population of CR3R in its boundary membrane and it is the fusion of this membrane with the plasma membrane that may represent the mechanism by which CR3 expression is increased. Preincubation of PMN with 10(-9)M rhTNF-alpha augmented phagocytosis, LTB4, and superoxide generation by PMN in response to activation by Z. In contrast, none of the responses to glucan was significantly increased after incubation with rhTNF-alpha. These differences suggest a lack of absolute homology between the recognition mechanisms for zymosan and glucan and that there is a component of the recognition mechanism for zymosan that is independent of that for glucan and is up-regulated after rhTNF-alpha pretreatment.

Glucans↗
PubMed1990

Zymosan-induced leukotriene B4 generation by human neutrophils is augmented by rhTNF-alpha but not chemotactic peptide.

Tumour necrosis factor (TNF) is a mediator of inflammation that has been shown to enhance neutrophil responses to soluble and particulate stimuli. The release of leukotriene B4 (LTB4) by human neutrophils stimulated by unopsonized zymosan was measured in the presence or absence of recombinant human TNF-alpha (rhTNF-alpha) preincubation. There was a threefold increase in the LTB4 response at an optimal TNF concentration of 10(-9) M and an optimal preincubation time of 10-20 min. A similar time and dose dependency was observed for CR3 receptor expression and for the release of the secondary lysosomal granule marker, vitamin B12-binding protein. In contrast, the chemotactic peptide formyl-methionyl-leucyl-phenylalanine (FMLP), although stimulating an increase in both CR3 receptor number and in particle phagocytosis, failed to induce an increase in LTB4 release in response to zymosan. In addition, the present study demonstrated that, unlike FMLP, the exocytotic mechanism for secondary granule release by rhTNF-alpha functioned in the absence of a rise in cytosolic free calcium. Furthermore, it was independent of changes in cyclic nucleotide concentrations and did not require an intact cytoskeleton. Thus the capacity of rhTNF-alpha to amplify the neutrophil response to zymosan through the CR3 receptor appears to be related to the amplification of post-membrane events as well as to an increase in the number of functionally active receptors.

Antigens, CD↗
PubMed1990

Nonspecific resistance-enhancing activity of zymosan in experimental bacterial infections.

The nonspecific resistance-enhancing activity of zymosan on experimental bacterial (Escherichia coli, Klebsiella pneumoniae, Proteus mirabilis, Pseudomonas aeruginosa, Serratia marcescens and Staphylococcus aureus) infections was investigated. Zymosan, being of very low toxicity, significantly enhanced nonspecific resistance to the above bacteria. The enhancement was the most pronounced 2 to 5 days after zymosan treatment.

Adjuvants, Immunologic↗
PubMed1990

Effect of oxidized phospholipids on the chemiluminescence of zymosan-activated leukocytes.

The effect of liposomes with different degree of oxidation on the zymosan-induced chemiluminescence (CL) of leukocytes was investigated. Non-oxidized liposomes did not influence significantly the CL response of leukocytes. In contrast previously oxidized liposomes increased CL even if liposomes and cells were separated by a dialysis membrane. Based on the observed increase of luminol-activated CL by oxidized liposomes, lipid peroxidation (LPO) products may be suggested to enhance cell activation. Zymosan-activated leukocytes did not affect the amount of malondialdehyde (MDA) in non-oxidized liposomes unless iron salts were added. Fe3+ + ADP added to non-oxidized liposomes triggered LPO. Both catalase and superoxide dismutase (SOD) prevented the effect. In experiments with previously oxidized liposomes the activated oxygen species produced by leukocytes did not increase the amount of MDA; on the contrary, they decreased it both in the presence and in the absence of chelated iron in the liposome suspension. The reaction between lipid hydroperoxide and O2- widely accompanied by CL. SOD decreased CL in this system by a factor of 1.7. On the other hand, peroxidized lipids may "opsonize" initially inactive particles: oxidized liposomes increased CL response of leukocytes similarly as opsonized zymosan routinely used as a phagocyte activator.

Humans↗
PubMed1990

Ethanol inhibits zymosan-stimulated and enhances nonstimulated platelet-activating factor production in a clonal macrophage cell line.

Ethanol was examined for its effects on zymosan phagocytosis and synthesis of platelet-activating factor (PAF) using a clonal macrophage cell line. PAF, identified as 1-O-alkyl-2-acetyl-sn-glycerol-3-phosphocholine, is a biologically active ether phospholipid produced by various cells types. PAF also activates a variety of inflammatory cells including the cells which produce PAF. Ethanol at 20 to 100 mM inhibited phagocytosis of unopsonized zymosan and concomitantly decreased PAF concentration in the stimulated macrophages. In contrast, in cells not stimulated with zymosan, ethanol increased the recoverable PAF. Ethanol, at 100 mM, inhibited the uptake of exogenous PAF but did not alter the distribution of PAF metabolites in the clonal macrophage cell line. The effect ethanol has on PAF synthesis appears dependent on the activation state of the cell. Two situations were identified in this study: 1) one linked to phagocytosis or cell stimulation which is inhibited by ethanol, and 2) PAF synthesis which is not dependent on overt cell activation that is enhanced by ethanol.

Animals↗
PubMed1989

Luminol dependent chemiluminescence of quartz and zymosan stimulated neutrophils.

The effect of the opsonization by zymosan and quartz particles on the chemiluminescence was investigated on human neutrophil granulocytes. Opsonization of zymosan enhanced the chemiluminescence response, while opsonized quartz inhibited the chemiluminescence reaction. Calcium ionophore A 23187 treatment did not influence the chemiluminescence of quartz but the light signal in the presence of quartz decreased rapidly. In parallel experiments the protein pattern of zymosan treated neutrophils was investigated by high resolution two-dimensional polyacrylamide gel electrophoresis.

Blood Proteins↗
PubMed1989

Isolation of a yeast heptaglucoside that inhibits monocyte phagocytosis of zymosan particles.

To isolate a unit ligand recognized by human monocyte beta-glucan receptors, acid-solubilized oligoglucosides were prepared by partial acid hydrolysis of purified yeast cell walls, gel filtered sequentially on Bio-Gel P-4 and P-2, derivatized with 2-aminopyridine, and separated by normal-phase HPLC. Ligand recognition was assessed by quantitating the effect of pretreatment with isolated materials on the capacities of adherent monocytes to phagocytose zymosan particles. Partial acid hydrolysis solubilized 23 +/- 4% (mean +/- SD; n = 7) of the cell wall glucans; at an input of 50 micrograms/ml, the solubilized products reduced the numbers of monocytes ingesting zymosan by an average of 44%. Gel filtration of acid-solubilized glucans on Bio-Gel P-4 revealed several peaks with phagocytosis-inhibiting activity, and fractions from the peak containing the smallest oligoglucosides, which accounted for 10 +/- 2% (mean +/- SD; n = 7) of the carbohydrate applied, were pooled. Further purification on Bio-Gel P-2 resolved this phagocytosis-inhibiting activity to a single peak that contained apparent heptaoses and accounted for 8 +/- 2% (mean +/- SD; n = 6) of the carbohydrate applied. At a concentration of 0.5 microgram/ml, the oligoglucosides pooled from the Bio-Gel P-4 and P-2 columns reduced the numbers of ingesting monocytes by 45 +/- 1% and 42 +/- 7% (mean +/- SD; n = 3), respectively. When derivatized with 2-aminopyridine, the oligoglucosides were resolved by HPLC to a number of peaks; a peak that eluted as an apparent heptaglucoside contained virtually all the inhibitory activity and accounted for only 6.6 +/- 0.7% (mean +/- SD, n = 7) of the carbohydrate applied. Gas chromatography analysis revealed only glucose and FAB-mass spectrometric analysis showed only heptaglucoside and no noncarbohydrate molecules. At a concentration of 1.6 ng/ml, the derivatized yeast heptaglucoside reduced the numbers of monocytes ingesting zymosan and glucan particles by 44 +/- 9% (mean +/- SD; n = 5) and 45 +/- 6% (n = 3), respectively. Thus, a heptaglucoside present in yeast cell walls is a unit ligand for human monocyte beta-glucan receptors.

Chromatography, Gel↗
PubMed1989

[Stimulation of nonspecific immune defense and antibody synthesis with zymosan].

A local sterile inflammation was induced in mice of different inbred strains by means of an i.p. injection of zymosan, a water-insoluble polysaccharide of the cell wall of Saccharomyces cerevisiae. This resulted in a strong enhancement of the unspecific resistance against infections with a LD 90 of gram-negative bacteria (Escherichia coli, Pseudomonas aeruginosa, Klebsiella pneumoniae and Bordetella bronchiseptica). Furthermore, the treatment with zymosan before or after an immunization with sheep erythrocytes (SE) resulted in a significantly increased specific IgM and IgG primary response in the spleen. However, it was particularly striking that the number of plaque-forming cells against SE was very drastically enhanced in non-immunized mice, in particular cases even up to more than 70 times over the background. Consequently, zymosan possesses immunomodulating effects both on the unspecific resistance and on immune reactions. These results are discussed in relation to the Lyt+-B-cells and an acute phase reaction of B-cells.

Animals↗
PubMed1987

Effects of herpesvirus infections on the chemiluminescence induced by zymosan phagocytosis in mouse peritoneal macrophages.

The chemiluminescence (CL) induced by zymosan phagocytosis was tested in mouse peritoneal macrophages infected with three different types of herpes viruses: herpes simplex type-1 (HSV-1), human cytomegalovirus (HCMV) and murine cytomegalovirus (MCMV). The intensity of CL was tested in various intervals of virus infections. In the first eight hours zymosan induced chemiluminescence decreased in all the three systems. By the 24th hour, the macrophages infected with HCMV had almost completely recovered from the early defect, while in the macrophages infected with both HSV-1 and MCMV, the chemiluminescence induced by zymosan remained impaired.

Animals↗
PubMed1986

Relative degradation of different arachidonoyl molecular species of choline glycerophospholipids in opsonized zymosan-stimulated rabbit alveolar macrophages.

The relative degradation of arachidonoyl molecular species of glycerophospholipids prelabeled with [3H]20:4 caused by opsonized zymosan was studied in rabbit alveolar macrophages using a recently developed high-performance liquid chromatographic method. The opsonized zymosan caused the release of [3H]20:4 only from choline glycerophospholipids, no significant changes being observed in the radioactivities of other glycerophospholipids and triacylglycerol. Choline glycerophospholipids were resolved into seven arachidonoyl molecular species, which differed as to the alkyl ether or acyl residue bound at the 1-position, by high-performance liquid chromatography. Arachidonate was predominantly located in the alkyl type having 16:0 at the 1-position which comprised more than half of the total arachidonoyl molecular species of choline glycerophospholipids. The radioactivities of all arachidonoyl molecular species of choline glycerophospholipids, except for the 18:2-20:4 and 18:1-20:4 species of diacylglycerophosphocholine, decreased to 80-85% of the control values as a result of the challenge with opsonized zymosan for 1 h. However, 50% of the released 20:4 came from the 16:0-20:4 species of alkylacylglycerophospholipids, which were the most predominant species of choline glycerophospholipids. The present results indicate that the 16:0-20:4 species of alkylacylglycerophosphocholine is a significant source of arachidonate and 1-O-alkyl-2-lysoglycerophosphocholine, the precursor of the platelet-activating factor, relative to other arachidonoyl species in activated alveolar macrophages.

Animals↗