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PubMed1991

Effects of repetitive bolus injections of zymosan-activated plasma on lung mechanics and airway responsiveness in awake sheep.

We studied the pulmonary effects of repetitive bolus injections of autologous zymosan-activated plasma (ZAP) in nine chronically instrumented awake sheep. Aerosol histamine responsiveness was determined 1 h before and 4.5 h after the first bolus injection of ZAP. Each sheep received in the pulmonary artery a total of eight 5-ml bolus injections of ZAP separated by 30 min. On a separate day, with the order of experimentation varied to avoid sequential bias, six of the nine sheep also received "control" plasma (plasma prepared in the identical fashion as ZAP but not incubated with zymosan). "Control" plasma caused reproducible transient increases in pulmonary artery pressure, but it did not cause alterations in any of the other measured variables. Repetitive bolus injections of ZAP caused reproducible alterations in lung mechanics, pulmonary hemodynamics, lung fluid and solute exchange, oxygenation, and peripheral leukocyte counts. The increases in thromboxane-B2 concentrations in lung lymph and plasma were greatest after the first bolus injection of ZAP, with the magnitude of these changes diminishing on succeeding injections of ZAP. Aerosol histamine responsiveness did not increase after the eight bolus injections of ZAP.

6-Ketoprostaglandin F1 alpha↗

PubMed1984

Glucocorticoid inhibition of zymosan-induced arachidonic acid release by rat alveolar macrophages.

The phospholipase-dependent liberation of arachidonic acid (AA) from membrane phospholipids has been proposed as the rate-limiting step in the synthesis of bioactive AA metabolites, which play an important role in the expression of inflammatory and immune reactions. We have examined the effects of steroids in vitro on the release of AA by rat alveolar macrophages exposed to zymosan. Fluocinolone (1 microM) significantly inhibited the zymosan-induced release of radiolabeled AA from phosphatidylcholine as well as the production of radiolabeled prostaglandin E2. (PGE2). Dose-response curves gave the following rank order of potency: fluocinolone greater than dexamethasone greater than hydrocortisone. The maximal degree of inhibition of radiolabeled AA release observed was approximately 70%. Inhibition was not observed after 3 h of glucocorticoid pretreatment, but maximal inhibition was achieved after 10 h of pretreatment. Pretreatment with gonadal sex hormones (1 microM) did not inhibit AA release. Concurrent incubation of macrophages with hydrocortisone and excess concentrations of the partial glucocorticoid agonist, progesterone, blunted the degree of inhibition observed with hydrocortisone alone. These data are consistent with a receptor-mediated process. The time course suggests a response dependent on new protein synthesis, and the increased concentration of the phospholipase-inhibitory protein, lipomodulin, in steroid-treated cultures is putative evidence of new protein synthesis.

Animals↗

PubMed2004

Delayed resolution of acute inflammation during zymosan-induced arthritis in leptin-deficient mice.

The severity of antigen-induced arthritis (AIA) is decreased in leptin-deficient ob/ob mice. However, joint inflammation in AIA depends on the immune response, which is impaired in ob/ob mice. In the present study we investigated the effects of leptin deficiency on zymosan-induced arthritis (ZIA), which is independent of adaptive immunity. Arthritis was induced by injection of zymosan into the knee joint. Joint swelling was similar after 6 and 24 hours in ob/ob and control mice. However, it remained elevated in ob/ob animals on day 3 whereas values normalized in controls. Histology revealed similar articular lesions in all animals on day 3, but on days 14 and 21 arthritis tended to be more severe in ob/ob mice. The acute phase response, reflected by circulating levels of IL-6 and serum amyloid A, was also more pronounced in ob/ob mice, although corticosterone was significantly elevated in these animals. Similar results were obtained in leptin receptor-deficient db/db mice. Thus, in contrast to AIA, ZIA is not impaired in leptin-deficient animals. On the contrary, resolution of acute inflammation appears to be delayed in the absence of leptin or leptin signalling, suggesting that chronic leptin deficiency interferes with adequate control of the inflammatory response in ZIA.

Acute Disease↗

PubMed1990

Pharmacological profile of alminoprofen among four writhing models of mice caused by kaolin, zymosan, acetylcholine and phenylquinone.

The effects of alminoprofen and other non-steroidal antiinflammatory drugs (NSAIDs) on the writhing reaction caused by kaolin, acetylcholine, phenylquinone and zymosan were studied. Aspirin, indomethacin, ibuprofen and diclofenac-Na, as cyclooxygenase inhibitors, showed similar potency ratios on four writhing tests, although, alminoprofen exhibited a somewhat rather higher potency ratio on kaolin- and zymosan-induced writhing models than on acetylcholine- and phenylquinone-induced writhing models. All NSAIDs, cyclooxygenase inhibitors except alminoprofen showed similar shapes in illustrations of potency ratio when the potency of aspirin was expressed as 1.0. The potency of alminoprofen produced a figure unlike those of other cyclooxygenase inhibitors. These results suggest that alminoprofen has a different pharmacological profile from other general NSAIDs in terms of analgesic action. This combination method with potency ratios for writhing reactions caused by the above four inducers could be a simple method for classification of pharmacological profiles of the analgesic actions of NSAIDs.

Acetylcholine↗

PubMed1990

Inhibition of superoxide generation and of increase in intracellular Ca2+ concentration by zinc in rat neutrophils stimulated with zymosan.

The effect of Zn2+ on the O2- generation and change in intracellular Ca2+ concentration ([Ca2+]i) of rat peritoneal neutrophils was studied. Zymosan (serum-treated zymosan (STZ))-induced O2- generation was inhibited by Zn2+ at concentrations as low as 10 microM. A large amount of the inhibition was observed in the absence of extracellular Ca2+ but the inhibition could not be restored by increasing the extracellular Ca2+ concentration, indicating that Zn2+ does not necessarily inhibit the O2- generation competitively with extracellular Ca2+. In the absence of extracellular Ca2+, Zn2+ inhibited STZ-induced transient increase in [Ca2+]i in the concentration range that evoked a marked inhibition in the O2- generation. On the other hand, Zn2+ did not inhibit significantly STZ-induced uptake of 45Ca2+ from extracellular medium by the cells. From these results, it is suggested that Zn2+ inhibits STZ-induced release of Ca2+ from intracellular storage sites, resulting in the suppression of the activation mechanism of neutrophils.

Animals↗

PubMed1985

Inhibitory effect of a novel anticomplementary agent, K-76COONa, on the release of histamine induced by zymosan and compound 48/80.

A novel sesquiterpene anticomplementary agent, K-76COONa, if locally applied, was revealed to have an activity to prevent histamine release from rat connective tissue mast cells not only in a zymosan-induced inflammation of the air pouch type (zymosan-air-pouch inflammation) but also in compound 48/80-induced air-pouch inflammation. Moreover, K-76COONa inhibited in vitro histamine release from rat peritoneal mast cells induced by compound 48/80.

Animals↗

PubMed1990

Human fibroblasts release low amounts of reactive oxygen species in response to the potent phagocyte stimulants, serum-treated zymosan, N-formyl-methionyl-leucyl-phenylalanine, leukotriene B4 or 12-O-tetradecanoylphorbol 13-acetate.

Cell lines of human fibroblasts from primary cultures released reactive oxygen species, and displayed an increase in low-level chemiluminescence when stimulated with serum-treated zymosan, N-formyl-methionyl-leucyl-phenylalanine, leukotriene B4, or 12-O-tetradecanoylphorbol 13-acetate, all of which are known stimulants of respiratory burst in phagocytic cells. Non-serum-treated zymosan, interleukin-6, interleukin-2, interferon-gamma or complement factor C3b were ineffective. The primary radical species produced was O theta.2. Radical formation was continuous for up to 4 h, and it did not occur as an oxidative burst. The low level chemiluminescence probably arose from the excitation of carbonyl groups, since it remained unchanged in the presence of azide and 1,4-diazabicyclo[2.2.2]octane. While the release of reactive oxygen species in phagocytes has a function in defense mechanisms, the sustained production of such species in tissue cells may have a role in signaling mechanisms. The amounts of reactive oxygen species released by the fibroblasts upon stimulation with the stimulants mentioned above were low in comparison with the known stimulatory effects of cytokines [Meier et al. (1989) Biochem. J. 263, 539-545].

Electron Spin Resonance Spectroscopy↗

PubMed1983

Zymosan-induced chemiluminescence of granulocytes in incubated human whole blood. The role of platelets.

Zymosan-induced chemiluminescence (ZI-CL) of whole blood which is mainly the response of granulocytes can be used as a rapid, simple and reliable diagnostic tool for hematological and allergic disorders. ZI-CL of whole blood remained unchanged when stored at 0 degree C for 4 hr, whereas it increased by incubation at 37 degrees C. This phenomenon points to platelet-granulocyte interaction during the incubation. ZI-CL of freshly prepared suspension of leukocytes and erythrocytes was enhanced by adding platelet rich plasma (PRP) obtained from incubated blood. Enhanced CL response was observed when erythrocytes or factors derived there of were present in incubated blood. Platelet stimulating factor (PSF) was prepared from incubated erythrocyte suspension. This factor also increased ZI-CL of granulocytes when incubated with fresh PRP. The consistent inhibition of CL of incubated blood by apyrase (0.5 U/ml) and the increased response of fresh blood by the addition of ADP (10(-5) M) suggested that this factor might be ADP itself. Platelets stimulated by this factor may respond more markedly to added zymosan for still unexplored reason with enhanced CL.

Adenosine Diphosphate↗

PubMed1985

Defective modulation of complement in Crohn's disease. C3b opsonization of zymosan by the alternative pathway.

Opsonization of zymosan by plasma complement was studied in 12 consecutive patients with untreated, well-established Crohn's disease and in 12 healthy volunteers. Binding of C3b to zymosan was markedly increased in patients with Crohn's disease during the first 30 min of the alternative pathway reaction, whereas consumption of the native C3 protein was within the normal range in all patients. Our results are consistent with a decreased capacity for degradation of activated C3,C3b by the I-H factor inactivator system. This immunologic abnormality may contribute to a chronic activation of the complement sequence, previously demonstrated in Crohn's disease, and to a release of split products of inflammation-promoting character.

Complement C3b↗

PubMed2001

Chronic type IV phosphodiesterase inhibition protects glomerular filtration rate and renal and mesenteric blood flow in a zymosan-induced model of multiple organ dysfunction syndrome treated with norepinephrine.

To examine the effects of chronic type IV phosphodiesterase (PDE4) inhibition on renal function and renal and mesenteric vascular resistance and blood flow in a sublethal model of multiple organ dysfunction syndrome (MODS) we used a prospective, randomized, controlled laboratory animal study. Twenty-eight rats had mini-infusion pumps placed to deliver vehicle or PDE4 inhibition with Ro 20-1724 at doses of either 0.3 or 2.0 microg/kg/min. Simultaneously, MODS was induced by intraperitoneal injection of zymosan (0.25 mg/g). Mean arterial blood pressure, heart rate, renal blood flow, and superior mesenteric blood flow (SMABF) were measured at 48 h. Renal vascular resistance (RVR), superior mesenteric artery vascular resistance (SMAVR), and glomerular filtration rate were calculated. A dose-response effect of norepinephrine was also evaluated at 48 h. Chronic Ro 20-1724 treatment prevented norepinephrine-induced vasoconstriction in control rats. Inhibition of PDE4 with Ro 20-1724 (2.0 microg/kg/min) increased urinary cAMP, and attenuated the increase in RVR and SMAVR (p < 0.05) and the decrease in RBF and SMABF (p < 0.05) that occurred from zymosan and norepinephrine. Glomerular filtration rate was also preserved (p < 0. 05), despite a reduction in blood pressure. Chronic PDE4 inhibition protects renal function and mesenteric perfusion during MODS by increasing cAMP in the presence and absence of catecholamines. Higher doses of PDE4 inhibition result in clinically tolerated decreases in mean arterial blood pressure, with improved end-organ function. Chronic PDE4 inhibition is protective, likely through cAMP-mediated attenuation of vasoconstriction.

3',5'-Cyclic-AMP Phosphodiesterases↗

PubMed2001

Role of mast cells in zymosan-induced peritoneal inflammation in Balb/c and mast cell-deficient WBB6F1 mice.

Zymosan-induced peritonitis was investigated in mast cell-deficient WBB6F1 mice and in Balb/c mice pretreated with mast cell stabilizer (cromolyn) or antagonists of histamine receptors (mepyramine, triprolidine, cimetidine, or ranitidine). The inherited mast cell deficiency in W/Wv knockouts of WBB6F1 mice impaired significantly the level of histamine and plasma exudation (measured 30 min after stimulation) as well as the influx of exudatory leukocytes, accumulation of plasma and exudate chemoattractants, and the release of proinflammatory cytokines (TNF-alpha, IL-1beta, and IL-6) measured at 6 h of inflammation. All of those factors were fully restored after selective intraperitoneal reconstitution of W/Wv mice with bone marrow-derived mast cells from their control +/+ counterparts. Cromolyn pretreatment of Balb/c mice reduced exclusively the early plasma exudation and histamine influx. Blocking of histamine receptors inhibited not only the early plasma exudation but also temporarily diminished primary leukocyte influx and levels of MCP-1 and IL-1beta. In conclusion, mast cells play an important role in the initiation of zymosan-induced peritonitis and modulate its further course.

Animals↗

PubMed2003

Exoenzyme Tat-C3 inhibits association of zymosan particles, phagocytosis, adhesion, and complement binding in macrophage cells.

Phagocytosis by macrophages is most important in the initial stages of an immune response. Although RhoA regulates cell adhesion, its roles in the integrin-related association of particles with macrophages and in phagocytosis are not clearly understood. We introduced C3 exoenzyme, a specific inhibitor of Rho, into J774A.1 macrophage cells fused with the 9 amino acid (49-57) transduction domain (RKKRRQRRR) of HIV-1 Tat. The presence of this Tat-C3 vector altered RhoA mobility on non-denaturing gels, indicating that Tat-C3 modified RhoA by ADP-ribosylation. Uptake of (FITC)-conjugated serum-opsonized zymosan particles and adhesion to fibrinogen-coated plates were reduced as was the association of serum-opsonized zymosan particles, and complement C3 and C3bi with the transfected cells. These results suggest that Rho regulates the activity of integrins that are involved in the association of particles with macrophages, phagocytosis, adhesion, and binding of complement C3 and C3bi.

ADP Ribose Transferases↗

PubMed2004

Effect of stobadine on opsonized zymosan stimulated generation of reactive oxygen species in human blood cells.

To predict more precisely the effect of stobadine, a pyridoindole antioxidant agent, in the whole organism, we studied its effect on opsonized zymosan-stimulated free radical generation in whole blood, on superoxide generation in the mixture of PMNL : platelets (1:50), as well as on superoxide generation and myeloperoxidase release in isolated PMNL. Without stimulation, stobadine had no effect on reactive oxygen species (ROS) generation and myeloperoxidase release. Stobadine in a concentration of 10 or 100 micromol/l significantly decreased luminol-enhanced chemiluminescence in opsonized zymosan-stimulated whole blood. In concentrations of 10 and 100 micromol/l, it reduced myeloperoxidase release from isolated neutrophils. Stobadine significantly decreased superoxide generation in isolated neutrophils in 100 micromol/l concentration. Its effect was much less pronounced in the mixture of neutrophils and platelets in the ratio close to physiological conditions (1:50). Our results suggest that stobadine might exert a beneficial effect in diseases or states where superfluous ROS generation could be deleterious.

Adult↗

PubMed1978

[Localization of N-acetyltransferases in sinusoidal liver cells. Effect of zymosan on the acetylation of sulfamethazine and isoniazid in the rat and in isolated perfused liver].

N-acetyltransferase (NAT) have been demonstrated to be localized in sinusoïdal cells and not in hepatocytes. Acetylation activities increased after pretreatment with Zymosan (40 mg/kg, i.v., 24 h before phenotyping) as well in vivo and in isolated perfused liver and in cytosolic fractions prepared from several rats organs. These data favor the localization of NAT-activity in reticulo-endothelial system. Increased protein levels in liver, gut, spleen and lungs cytosolic fractions (100 000 g, 120 mn) 48 h after Zymosan administration, suggest and inducing effect of this drug on NAT activity.

Acetylation↗

PubMed1991

[The action of trypsin and zymosan on the respiration of cultivated endothelial cells].

Trypsin and Zymosan induce an increase in respiration activity of cultivated endothelial cells. These effects are not due to the production of oxygen radicals. The effect of trypsin will be explained by interfering with the cellular homeostasis of calcium. The stimulated respiration after incubation with zymosan may be connected with the increased phagocytosis.

Animals↗

PubMed1990

Binding of the pentamer/hexamer forms of mannan-binding protein to zymosan activates the proenzyme C1r2C1s2 complex, of the classical pathway of complement, without involvement of C1q.

The serum lectin, mannan binding protein (MBP), was isolated in a yield of 40 micrograms/liter from pooled normal human serum by affinity chromatography on mannan-Sepharose, followed by gel-filtration and ion-exchange chromatography and finally by passage down an anti-IgM Sepharose column. A rabbit antiserum was prepared against the purified MBP and an enzyme-linked immunoassay developed that used both the specificity of the polyclonal antibody and the Ca+(+)-dependent carbohydrate binding property of MBP. Assay of the sera from 103 blood-donors showed a wide range of MBP levels, ranging from 0 to 870 micrograms/liter. MBP, after interaction with zymosan, caused efficient activation of a C1r2 125I-C1s2 complex that was prepared by incubation of 125I-C1s2 with serum, from a patient with a complete genetic deficiency of C1q, followed by gel-filtration on Sepharose 6B. The purified MBP is composed of a mixture of trimers, tetramers, pentamers, and hexamers of an approximate 90-kDa structural unit as judged by chromatography, SDS-PAGE and electron microscopy studies. Only the molecules in the pentamer/hexamer fraction, which have a similar overall structure to that of C1q, appeared to cause efficient, zymosan-dependent, activation of C1s within the C1r2C1s2 complex. The pentamer/hexamer form of MBP may therefore play an important role in antibody-independent activation of the C system during the early stages of certain infections.

Calcium↗

PubMed1988

Fibronectin enhances respiratory burst of phagocytes stimulated by zymosan and immune complexes.

Plasma fibronectin (FN) has been demonstrated to serve as an opsonin involved in the ingestion of foreign particles by phagocytes. This study concerns the effect of FN exposure on the respiratory burst of normal human peripheral phagocytes, using a luminol-dependent chemiluminescence (CL) assay for measurement of reactive oxygen metabolites generated. FN enhanced, in a dose-dependent manner, the CL response of circulating monocytes stimulated, probably via beta-glucan receptor, with unopsonized zymosan. FN also increased the CL response of phagocytes to fresh serum-opsonized zymosan. When we used a glycolipid (ceramide pentasaccharide, CPS) incorporated on liposome membranes as an antigen, the immune complexes prepared between CPS and human IgG (as antibody) did not induce a CL response, differing from previous reports. Addition of FN to the immune complexes significantly enhanced the CL response of phagocytes. The role of FN in host defence is discussed.

Antigen-Antibody Complex↗

PubMed1988

Synergism between zymosan-activated serum and heparin in the induction of polymorphonuclear leukocyte aggregation.

During the course of extracorporeal circulation, leukocyte aggregation is known to occur in some patients. This is attributed to complement activation and release of the chemotactic factor C5a. We investigated the effect of heparin on in vitro complement induced aggregation of polymorphonuclear leukocytes (PMNAGG), since most patients undergo heparinization during the extracorporeal circulation. Our results indicate that sub-aggregating concentrations of zymosan-activated serum (ZAS) enhance heparin-induced PMNAGG and that sub-aggregating amounts of heparin increase the aggregation induced by ZAS. Heat inactivation of the serum prior to zymosan activation abrogated the aggregating activity of the ZAS. Furthermore, the combined ZAS and heparin-induced PMNAGG was partially inhibited by specific antibodies to C5a but not to C3a. Therefore, we suggest that heparin and C5a may have a synergistic effect on the aggregation of polymorphonuclear leukocytes. These data might be relevant to situations in which patients are subjected to extracorporeal circulation.

Cell Aggregation↗