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PubMed1992

A nonlethal intravenous dose of endotoxin influences opsonized zymosan-stimulated [32P]phospholipid turnover in rat alveolar macrophages.

The opsonized zymosan-stimulated turnover of 32P-labeled phospholipids was examined in alveolar macrophages from rats 3 hr after intravenous administration of saline or a nonlethal dose of endotoxin. Stimulation resulted in increased incorporation of [32P]PO4 into phosphatidic acid and phosphatidylinositol. Also a decreased [32P]phosphatidylcholine and an increased [32P]lysophosphatidylcholine labeling were observed, suggesting an increased activity of phosphatidylcholine-specific phospholipase A2. Endotoxin attenuated these changes in 32P-labeled phospholipids, demonstrating the ability of a nonlethal dose of endotoxin to perturb phospholipid-dependent signal transduction mechanisms in cells isolated from a compartment other than the one in which endotoxin was administered.

Animals↗
PubMed1991

Neutrophil chemiluminescence and superoxide production in patients with rheumatoid arthritis: the effect of zymosan, phorbol myristate acetate and platelet-activating factor.

Previous study demonstrated that platelet activating factor (PAF) was a potent inducer of polymorphonuclear leukocyte (PMN) activation. This study used a luminometer to measure the chemiluminescence (CL) of peripheral blood (PB) PMNs in 15 patients with rheumatoid arthritis (RA). Superoxide production from PB and synovial fluid (SF) PMNs was also determined by inhibiting reduction of ferricytochrome C with superoxide dismutase. Neutrophils obtained from 12 age- and sex-matched healthy subjects (HS) were used as controls. The results showed that PAF at both 1 microM and 10 microM significantly increased neutrophil CL in both RA (1.40 +/- 0.90 mv, 1.87 +/- 1.18 vs control 0.66 +/- 0.18) and HS (1.70 +/- 0.72, 2.22 +/- 1.25 vs control 0.67 +/- 0.13), with no significant difference between the two groups. Both PMA and zymosan also significantly enhanced PMN CL in both RA (41.51 +/- 17.42, 40.0 +/- 26.51) and HS (43.42 +/- 17.28, 39.91 +/- 27.24), and those values were much higher than those of controls or via PAF stimulation, but, again, there was no difference between RA and HS groups. Lipopolysaccharide (LPS)-stimulated mononuclear cell supernatant can induce neutrophil activity, too. Like CL, PAF had a weak effect on the generation of superoxide from PMNs. Neutrophils from seven RA SF stimulated with PMA or PAF showed a significant increase in superoxide production (76.05 +/- 2.14, 2.83 +/- 0.18) and these were higher than in PB of either RA patients (54.35 +/- 12.46, 1.03 +/- 0.74) and HS (55.70 +/- 17.9; 1.08 +/- 1.12) (p less than 0.05). These findings demonstrated the PMNs were more activated in SF than those in PB of RA patients and HS, suggesting some unidentified factors in SF provoked PMNs activation.

Arthritis, Rheumatoid↗
PubMed1991

[Rat multiple organ failure model caused by zymosan injections: a pathomorphological study].

We succeeded in developing a Wistar rat multiple organ failure (MOF) model by intraperitoneal injection of Zymosan. 80 rats were divided into the experimental and control groups. On alternative days (1, 2, 4-5 day), rats were killed after their blood specimens were examined. In the experimental group, changes in PaO2, GPT and Cr were apparently significant as compared with those in the control group. Symptoms included lethargy, hyporeaction, and alimentary tract hemorrhage. By combining function with pathology changes at the cellular and subcellular level and histochemical aspects, we listed MOF pathological features for the diagnosis of DIC at its different stages.

Animals↗
PubMed1991

Inhibition of cellular immune reactions by zymosan.

Mice treated intraperitoneally with zymosan showed a strong inhibition of the DTHR (delayed-type hypersensitivity reaction) against sheep erythrocytes (SE), ovalbumin (OA), and alloantigen. Furthermore, the rejection time of skin transplants was nearly doubled while antibody formation against SE was significantly enhanced. When a DTHR against OA and an antibody formation against SE were induced at the same time in the same animals, than the suppressive and stimulating effects cancelled each other. These results are discussed with regard to the sensitivity of lymphocyte subpopulations, which may be different if exposed to phagocytosis-induced oxygen radicals.

Animals↗
PubMed1989

Changes of immunological parameters in immunocompromised patients under selective decontamination of the digestive tract. Second Part: Investigations on the influence of drugs on zymosan-induced and luminol-enhanced chemiluminescence of peripheral leucocytes.

The influence of drugs used for selective decontamination, given in therapeutically effective concentrations, was examined in healthy controls and immunocompromised patients with hematologic systemic diseases by measuring the zymosan-induced and luminol-enhanced chemiluminescence of peripheral leucocytes. Drug-induced repression of phagocytic activity could usually be found both in healthy controls and in patients with hematologic systemic diseases. The combination of trimethoprim and sulfamerazine had a pronounced repressive effect. Such indications should be taken as a basis for further investigations in order to avoid additional iatrogenic restriction of defence. If possible, drugs with effects leading to repression of phagocytosis should not be used for selective decontamination.

Anti-Infective Agents↗
PubMedDate not supplied

Inhibition of the zymosan-induced chemiluminescence of human phagocytes by adenosine, polyadenylic acid and agents influencing adenosine metabolism.

The zymosan-induced chemiluminescence of human phagocytes (neutrophil granulocytes) could be inhibited by adenosine, polyadenylic acid, dipyridamole (an agent blocking the cellular adenosine uptake) and coformycin (a highly potent inhibitor of enzyme adenosine deaminase). It is suggested that in estimating the antianginal and antithrombotic action of dipyridamole, its action on the phagocytes should be taken into account. The same consideration would be true for 2'-deoxycoformycin (a coformycin analogue) used as a potent anticancer and immunosuppressive drug.

Adenosine↗
PubMed1989

[Lipid peroxidation reactions to the administration of various doses of zymosan].

The results have been presented of the zymosan (Z) effect mechanism in the reaction of the lipid peroxidation and the parts' separation of the protection antioxidant. The experiments were made on 32 Wistar rats. At the experimental series 25 mg/kg and 100 mg/kg of Z were injected. Control rats were injected with physiological saline alone.

Animals↗
PubMed1989

Effects of ketoprofen and indomethacin on leukocyte migration in two models of pleurisy induced by carrageenan or zymosan-activated serum in rats.

The effect of nonsteroidal anti-inflammatory drugs on the in vivo leukocyte migration is not understood fully. In the present study, the effects of indomethacin and ketoprofen on the intrapleural leukocyte accumulation induced by carrageenan or zymosan-activated serum (ZAS) were investigated. Rats were given indomethacin or ketoprofen p.o. (1, 3 or 9 mg/kg) 1 hr before intrapleural injection of carrageenan (1 mg) or ZAS (0.5 ml). Pleural exudates were harvested 4 hr later. In each model of pleurisies, ketoprofen and indomethacin reduced the volume of exudate and leukocyte count in a dose-dependent manner but ketoprofen was more active than indomethacin. Ketoprofen and indomethacin had no effect on the protein concentration and the total complement activity of the exudates induced by carrageenan or ZAS. The spontaneous and directed migrations of leukocytes elicited by ZAS were unaffected by indomethacin and ketoprofen, whereas those of leukocytes elicited by carrageenan were more inhibited by ketoprofen than by indomethacin. These data demonstrate that ketoprofen is more active than indomethacin in reducing the in vivo leukocyte migration evoked by carrageenan or ZAS and suggest that the main effect of these two drugs is to reduce the increase in vascular permeability. Neutrophil chemotactic responsiveness and generation of chemotactic factors alone cannot explain the anti-inflammatory effect of ketoprofen and indomethacin.

Animals↗
PubMed1985

Membrane complement receptor type three (CR3) has lectin-like properties analogous to bovine conglutinin as functions as a receptor for zymosan and rabbit erythrocytes as well as a receptor for iC3b.

Human leukocyte complement receptor type three (CR3) was shown to be lectin-like and to resemble bovine serum conglutinin (K) in that it bound to both iC3b and unopsonized yeast (Saccharomyces cerevisiae), and was inhibited by EDTA or N-acetyl-D-glucosamine (NADG). CR3 and K also bound to zymosan (Z), a yeast cell wall extract that contains primarily polysaccharide and no detectable protein. However, structural differences and the absence of K on bovine phagocytes indicated that CR3 was not the human homologue of bovine K. Phagocytic and respiratory responses to unopsonized Z were CR3 dependent because they were inhibited by monoclonal antibodies specific for the alpha-chain of CR3 and did not occur with phagocytes from patients with a genetic deficiency of CR3. The binding of CR3 to Z did not require opsonization of the Z with neutrophil-secreted C3, as Z binding and responses were not inhibited by Fab anti-C3. In addition, CR3-dependent binding of yeast occurred with neutrophils from which protein secretion was blocked by fixation with paraformaldehyde. Rabbit erythrocytes (RaE) also bound weakly to neutrophil CR3 and triggered ingestion. Anti-CR3 not only blocked the binding and ingestion of RaE but also blocked selectively the ingestion of RaEC3b without affecting the strong binding mediated by CR1. Even though sheep E and sheep EC3b were not ingested by neutrophils, a weak binding of CR3 to sheep E was suggested by the finding of 20 to 40% inhibition of sheep EAIgG ingestion by anti-CR3. Such inhibition was only observed in buffers that allowed activity of the CR3 binding site and not in buffers containing either EDTA or NADG. An apparently contradictory finding was that the weak CR3-dependent binding of Z triggered neutrophil ingestion and a superoxide burst, whereas the avid CR3-dependent binding of sheep EC3bi did not induce significant ingestion or a respiratory burst. Blocking studies with monoclonal antibodies specific for different epitopes of the alpha-chain of CR3 suggested that this might result from the presence of two distinct binding sites in CR3: one site for fixed iC3b that did not trigger functions, and a second function-triggering site for Z that did not bind to fixed iC3b.

Animals↗
PubMed1987

Interferon-alpha enhances the production of leukotriene B4 in murine peritoneal macrophages stimulated by opsonized zymosan.

Murine peritoneal macrophages pretreated with interferon (IFN)-alpha and then stimulated by opsonized zymosan produced two to three times more LTB4 than untreated macrophages. However, PGE2 production was not changed by IFN-alpha. Meanwhile, IFN-gamma did not affect the production of LTB4 and PGE2. From the results it is considered that IFN-alpha can modulate inflammation or host defence through the production of LTB4.

Animals↗
PubMed1988

Pulmonary effects of zymosan activated plasma and phorbol myristate acetate in anaesthetized and awake rabbits.

The ability of two polymorphonuclear granulocyte (PMN) activators, Zymosan activated plasma (ZAP) and Phorbol myristate acetate (PMA), to induce an adult respiratory distress syndrome (ARDS) type lung injury was compared in awake and anaesthetized rabbits. The preparatory procedure itself decreased the concentrations of circulating PMN and lymphocytes in anaesthetized animals. ZAP acutely lowered the number of circulating leukocytes due to a fall in PMN only, this was followed by a rebound. Both effects were more marked in awake than in anaesthetized animals. PMA caused a virtual disappearance of both PMN and lymphocytes from the blood. There was no rebound, and no difference between anaesthetized and awake animals. The activators caused equal increases in pulmonary arterial pressure (about 0.67 kPa) initially. This was followed by a return to baseline in ZAP animals, but a further increase in those given PMA. Increased airway pressure (0.4 kPa) was seen only in the PMA group; PaO2 decreased only in awake rabbits given PMA. Both activators, as well as the preparatory procedure itself, caused PMN accumulations in the alveolar septa, septal thickening, and modest perivascular edema with intact tissue architecture. PMA caused the most marked changes. Wet/dry lung weight ratios were only moderately increased. In conclusion, ZAP and PMA had different effects on circulating leukocytes, but gave nearly the same degree of PMN accumulation in the lungs. The modest edema indicated some increased microvascular leakage, but a fully developed ARDS-type lung injury did not occur.

Anesthesia↗
PubMed1977

Interaction of zymosan and of activated properdin with factor D-depleted guinea pig serum: implications for the mechanism of initial C3 cleavage via the alternative complement pathway.

Factor D of the alternative C pathway was specifically removed from guinea pig serum. The resulting serum reagent (RD) supported neither the formation of a C3-cleaving enzyme on zymosan (Z) nor the inactivation of C3 or of factor B in the presence of Z or activated properdin (P). Addition of purified D to RD restored these properties. Studies were limited amounts of purified D were added to RD with Z or P as activating substances, gave the following results: (1) Inactivation of B and of C3 occurs in the presence of minute amounts of D. (2) C3 inactivation is more efficient than B inactivation and proceeds even in the absence of detectable enzymatic B activation. (3) C3 cleavage at any D concentration tested is always accompanied by uptake of C3 fragments onto Z. With respect to initial C3 cleavage via the alternative C pathway these data suggest that the initiating reaction is D-dependent, very efficient in depositing C3 fragments on particulate activating substances such as Z and able to utilize factor B in an apparently uncleaved form.

Animals↗
PubMed1978

Responses of human platelets to immunologic stimuli: independent roles for complement and IgG in zymosan activation.

Analysis of the zymosan (Z)-induced human platelet response with washed platelets, fresh agammaglobulinemic plasma, and purified human IgG has identified a previously unrecognized role of IgG in this reaction, in addition to the previously reported requirements for C and fibrinogen. The rate-limiting step involves the assembly of C components on the Z particles and is independent of immunoglobulin. After the heat-labile components (supplied by agammaglobulinemic plasma) are Z bound, Z-specific IgG (apparently antibody) can bind to Z very rapidly, conferring on the previously inactive Z-complement-fibrinogen intermediate the capacity to induce platelet aggregation and serotonin release. The critical function of this Z-bound IgG appears to be in the interaction of the active Z complex with the platelet through Fc receptors, since soluble Fc fragments of each IgG subclass can totally block platelet activation. It is proposed that the human platelet requires a dual, or multi-site, stimulation to become activated during some forms of immunologic injury. These findings may provide some insight into clinical syndromes involving thrombocytopenia and intravascular coagulation during sepsis.

Agammaglobulinemia↗
PubMed1983

The stimulation of superoxide anion production in guinea-pig peritoneal macrophages and neutrophils by phorbol myristate acetate, opsonized zymosan and IgG2-containing soluble immune complexes.

The kinetics of superoxide anion production in guinea-pig peritoneal macrophages and neutrophils were determined following in vitro stimulation with phorbol myristate acetate (PMA), opsonized zymosan (OZ) and soluble immune complexes of guinea-pig IgG2 (SIC). Superoxide production was recorded as chemiluminescence (CL) arising from the reductive cleavage of lucigenin. With PMA, both macrophages and neutrophils displayed a two-phase response consisting of a rapid initial burst of CL, which preceded ligand ingestion, followed by a plateau in the CL response which persisted for more than 30 min. By contrast, OZ induced a slow progressive increase in CL in both phagocytes which was consistent with the development of an oxidative burst concomitant with ingestion. The phagocytes differed in their responses to SIC, the macrophages displaying CL kinetics similar to those observed with PMA, whereas the neutrophils responded in the manner observed with OZ. The relationship between disparity in the patterns of macrophage and neutrophil CL responses to SIC and differences in their expression of Fc receptors for IgG2 (Coupland & Leslie, 1983) is discussed.

Animals↗
PubMed1983

Release of leukotriene B4 from human neutrophils and its relationship to degranulation induced by N-formyl-methionyl-leucyl-phenylalanine, serum-treated zymosan and the ionophore A23187.

The release of leukotriene B4 (LTB4) from human neutrophils and its relationship to degranulation induced by the divalent cation ionophore A23187, serum-treated zymosan (STZ), N-formyl-methionyl-leucyl-phenylalanine (FMLP) and arachidonic acid (AA) have been studied. Greatest release of LTB4, measured by specific radioimmunoassay, occurred in response to A23187 (5-10 ng/10(6) cells); lower concentrations were obtained after incubation with STZ (0.2-0.8 ng/10(6) cells) and AA (0.3-2.6 ng/10(6) cells) and low (0.02 ng/10(6) cells) or not detectable amounts from cells incubated with FMLP. Release of LTB4 induced by STZ, FMLP and submaximal concentrations of A23187 was potentiated by simultaneous addition of AA. Lower amounts (0.06-0.3 ng/10(6) cells) of thromboxane B2 (TXB2) were also released by these stimuli, however this release of TXB2 was not potentiated by exogenous AA. The secretion of beta-glucuronidase induced by A23187, STZ and FMLP was not quantitatively related to release of LTB4 or TXB2 and was not potentiated by exogenous AA. Furthermore, FMLP induced degranulation was cytochalasin B (Cyt B)-dependent, whereas LTB4 release in response to this stimulus was only marginally increased by pretreatment of the cells with Cyt B. These data indicate that LTB4 does not mediate degranulation induced by these stimuli.

Anti-Bacterial Agents↗
PubMed1984

Differential activation of phosphatidylinositol deacylation and a pathway via diphosphoinositide in macrophages responding to zymosan and ionophore A23187.

The inositol phospholipids of peritoneal macrophages were prelabeled with [3H]inositol to enable studies on the enzymatic mechanisms of stimulus-induced phosphatidylinositol breakdown. Ionophore A23187 induced a rapid breakdown of phosphatidylinositol in the presence of Ca2+ with 25% loss occurring within 5 min. The main water-soluble product of this breakdown was identified as inositol diphosphate. Since the accumulation of inositol diphosphate far exceeded the concomitant decrease in polyphosphoinositides, an increased phosphorylation of phosphatidylinositol must have preceded, or accompanied, the degradation of diphosphoinositide. The degradation of phosphatidylinositol induced by A23187 was shown to be strictly dependent on Ca2+. The monovalent cation ionophore monensin and platelet-activating factor increased the level of diphosphoinositide but caused no net degradation of inositol phospholipids. The same effect was seen with ionophore A23187 in the absence of Ca2+. Zymosan particles also induced extensive degradation of phosphatidylinositol. Products of phosphodiesterase-catalyzed cleavage of inositol lipids were observed, but the pathway of deacylation dominated as evidenced by the accumulation of lysophosphatidylinositol and glycerophosphoinositol. Deacylation was also enhanced in response to concanavalin A. Thus, in mouse peritoneal macrophages phosphatidylinositol breakdown occurred primarily by deacylation or via diphosphoinositide, depending on the stimulus, rather than through a phosphatidylinositol phosphodiesterase reaction.

Animals↗