Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “ZYMOSAN”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 523 records · Page 29Linked to original sources
PubMed1989

Neutrophil kinetics in rabbits during infusion of zymosan-activated plasma.

Complement activation in vivo produces neutropenia and pulmonary sequestration of neutrophils (PMNs) whereas in vitro activation increases PMN adherence and decreases PMN deformability. The present study examined PMN kinetics in vivo to determine if this sequestration was specific to the lung. Venous or arterial injections of radiolabeled PMNs were given to animals receiving infusions of zymosan-activated plasma (ZAP) or saline, and the PMN distribution was evaluated 10 min later. In control animals, the relative size of the marginated and circulating PMN pools was similar after venous or arterial injection and regional PMN retention increased as blood velocity slowed. ZAP infusion produced threefold increases in PMNs within pulmonary capillaries after venous injection and PMN retention was independent of blood velocity. After arterial injection, ZAP infusion produced PMN sequestration in all organs. Rigid (glutaraldehyde-fixed) PMNs injected into control rabbits showed increased lung recoveries similar to those of fresh PMNs injected into ZAP-treated rabbits. We conclude that activation of the complement system causes PMN sequestration in both the pulmonary and the systemic microvasculature and that the decrease in PMN deformability that occurs with activation of the PMN may be important in the genesis of PMN sequestration.

Animals↗
PubMed1989

Zymosan-activated plasma causes prolonged decreases in PMN superoxide release in sheep.

It is well established that activation of neutrophils within the pulmonary circulation produces acute lung injury in which adherence of neutrophils to endothelial cells is an obligatory step in the mechanism of injury. The effects of in vivo activation of neutrophils on the in vitro responses of these cells to stimulation have not been determined, although such information may be important in understanding how different etiological factors may interact to produce infection or acute respiratory failure. By using an assay to sequentially measure superoxide anion (O2-) release from adherent neutrophils stimulated with phorbol myristate acetate (PMA), we measured the in vitro activation response of peripheral blood neutrophils isolated before and 24 h after infusion of zymosan-activated plasma (ZAP; or untreated plasma as a control), air bubbles, or PMA in awake, instrumented sheep. Each of the three inflammatory agents produced an increase in lung microvascular permeability characteristic of acute lung injury; control plasma did not. For the in vivo ZAP experiments, stimulated O2- release in vitro by using PMA was approximately 50% lower (P less than 0.05) for neutrophils isolated 24 h after the in vivo infusion (4.3 +/- 0.8 nmol/500,000 cells) than before (8.1 +/- 0.2 nmol/500,000 cells). For the air emboli or PMA in vivo experiments, there were no changes in neutrophil activation responses in vitro. Similarly, infusion of control plasma did not result in reduced neutrophil O2- release. These results show that alterations in the inflammatory potential of neutrophils may occur in vivo and that such alterations appear to be dependent on the mechanism and agent by which lung injury is produced.

Animals↗
PubMed1992

Effect of zymosan-activated plasma on the deformability of rabbit polymorphonuclear leukocytes.

Intravascular infusion of inflammatory mediators causes a sudden neutropenia due to the sequestration of polymorphonuclear leukocytes (PMN) within the microvasculature of the lung and other organs. This sequestration could be due to a decrease in the ability of PMN to deform and pass through the narrow capillary bed. The purpose of this study was to determine if the complement fragments present in zymosan-activated plasma (ZAP) caused a rapid stiffening of PMN. The PMN deformability was determined by measuring the pressure required to pass PMN through a polycarbonate filter containing 5-micron pores at a constant flow rate as well as the extraction of PMN compared with red blood cells and 125I-labeled albumin by the filter. The role of the cytoskeleton in PMN deformation was examined in studies where F-actin formation was inhibited using cytochalasin B or microtubule assembly was inhibited using colchicine. The results showed that treatment with ZAP induced a rapid decrease in PMN deformability. Inhibiting the formation of F-actin made the unstimulated PMN more deformable and reduced the stiffening induced by ZAP. In contrast, inhibition of microtubule reassembly did not alter either normal deformability or the ZAP-induced decrease in deformability. In vivo, colchicine increased normal PMN margination but did not inhibit the rapid sequestration of PMN induced by infusion of ZAP. These studies indicate that ZAP induces a rapid decrease in PMN deformability that is mediated through the cytoskeleton. They suggest that this decrease is due to the polymerization of F-actin.

Actins↗
PubMedDate not supplied

Trypanosoma cruzi Infection Impairs the Endocytosis of Zymosan A by Cardiomyocytes.

OBJECTIVE: We have previously reported that mannose receptors participate and are regulated during Trypanosoma cruzi cardiomyocyte (CM) infection. Our present aim is to characterize the endocytosis of mannosylated ligands like zymosan A (Zy) in uninfected and T. cruzi-infected CM. METHODS: CM infected or not by T. cruzi were incubated with Zy for different periods of time and their internalization was analyzed at light microscopy level. Fluorescent approaches were performed by treating Zy with concanavalin-A-TRITC and washing it exhaustively prior to incubation with CM. The cultures were further stained with phalloidin-FITC and DAPI for actin and DNA visualization, respectively. RESULTS: CM internalized Zy particles in a time-dependent fashion. The ligand specificity was confirmed by the addition of mannan, which efficiently blocked the Zy endocytosis. Designed fluorescent approaches extended and confirmed the Zy internalization by striated cells. Infected cultures displayed impairment in Zy endocytosis, which seems to be directly related to host infection rates. CONCLUSIONS: Altogether, our results show the ability of CM to ingest large particles such as the mannosylated ligand Zy. During their infection with T. cruzi, there is a loss in Zy internalization possibly due to the negative modulation of mannose receptors.

Animals↗
PubMed1977

C3 and C5-cleaving properdin enzymes formed on zymosan incubated with human serum: the decay and the regeneration of the enzymes.

Incubation os zymosan (Z) with normal human serum led to the formation of ZXhu, which had the abilities to cleave C3 and C5. Kinetic studies on ZXhu formation revealed that the amount of inactivated C5 by ZXhu, when expressed in site-forming unit (SFU), was much greater than that of inactivated C3. When ZXhu having limited C3 and C5-cleaving was incubated at 37 degrees C it decayed with a first order reaction completely in 120 min. At any stage of decay of ZXhu, the activities could be restored by the addition of both B and D, but not by the addition of B or D alone. Not D but B could be bound to the completely decayed ZXhu, and activation of bound B by D led to the regeneration of ZXhu.

Beta-Globulins↗
PubMed1992

Lung oxidant changes after zymosan peritonitis: relationship between physiologic and biochemical changes.

Our purpose was to determine the effect of non-bacteria-dependent systemic inflammation on the degree and time course of lung oxidant activity and antioxidant defenses, comparing these changes with lung, physiologic, and histologic alterations. Adult male rats were given intraperitoneal zymosan (0.7 mg/g body weight) and were fluid resuscitated. Oxidant changes were measured as lung tissue oxidized glutathione (GSSG) and malondialdehyde (MDA) content, antioxidant defenses as tissue reduced glutathione (GSH), and catalase. Animals were killed at 4, 12, and 24 h, and at 5, 10, and 30 days. Lung data were compared with that found in liver. We noted a 45% mortality in the first 18 to 36 h with all remaining animals surviving. In the first 24 h, we noted a doubling of lung MDA and an 80% conversion of tissue GSH to GSSG compared with less than 5% in control animals, indicating a severe oxidant stress. These findings corresponded with marked increase in lung neutrophils. Arterial pressure (PaO2) was significantly decreased from a control of 95 +/- 4 mm Hg to 80 +/- 5 mm Hg and 75 +/- 4 mm Hg at Days 5 and 10, respectively, but returned toward control by 30 days. Lung GSSG and MDA remained significantly increased for the 30-day period, whereas amounts of the antioxidants, catalase, and GSH returned to control after 24 h. The ongoing oxidant stress corresponded with marked mononuclear cell infiltration and interstitial thickening, which persisted over the 30-day period even after peritonitis had completely resolved.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2004

PTX3 function as an opsonin for the dectin-1-dependent internalization of zymosan by macrophages.

Pentraxin 3 (PTX3) is a tumor necrosis factor and interleukin-1beta-stimulated gene that encodes a long PTX with proinflammatory activity. Here, we show that peritoneal macrophages derived from PTX3 transgenic (Tg) mice express higher levels of PTX3 mRNA than macrophages from wild-type (WT) mice, at basal level as well as upon stimulation with zymosan (Zy). Macrophages from Tg mice also showed improved opsonin-independent phagocytosis of Zy particles and the yeast form of the fungus Paracoccidioides brasiliensis. In the case of P. brasiliensis, an enhanced microbicidal activity accompanied by higher production of nitric oxide was also observed in macrophages from Tg mice. Using fluorescein-activated cell sorter analysis and reverse transcriptase-polymerase chain reaction, we demonstrated that basal level of Toll-like receptor-6 and Zy-induced dectin-1 expression was slightly but consistently higher in macrophages from Tg mice than in macrophages from WT mice. Recombinant (r)PTX3 protein binds to Zy particles as well as to yeast cells of P. brasiliensis and addition of rPTX3, to a culture of WT-derived macrophages containing Zy leads to an increase in the phagocytic index, which parallels that of Tg-derived macrophages, demonstrating the opsonin-like activity of PTX3. It is important that blockade of dectin-1 receptor inhibited the phagocytosis of Zy particles by WT and PTX3 Tg macrophages, pointing out the relevant role of dectin-1 as the main receptor involved in Zy uptake. Our results provide evidence for a role of PTX3 as an important component of the innate-immune response and as part of the host mechanisms that control fungal recognition and phagocytosis.

Animals↗
PubMed1993

Serum components induce beta-D-glucan-inhibitable uptake of zymosan particles by murine peritoneal macrophages.

Effects of murine serum (NMS) treatment on (1-->3)-beta-D-glucan inhibitable uptake of zymosan particles (ZYM) (GIZUP) by murine peritoneal macrophages (PM) and the structural specificity of the inhibition were examined. ZYM uptake by PM treated with NMS was enhanced in comparison with those treated with medium, and in a concentration- and incubation time-dependent manner. The enhanced ZYM uptake was significantly reduced by the pretreatment of PM with soluble (1-->3)-beta-D-glucans. These facts suggest that NMS enhances GIZUP. The effect disappeared by the treatment of NMS with gelatin-Sepharose which removed fibronectin (FN) from the serum, suggesting a significant contribution of FN on GIZUP. In addition, the administration of beta-glucan in vivo elevated the concentration of FN in serum by acute phase response and enhanced GIZUP, suggesting the positive contribution of acute phase responses on beta-glucan mediated immunopharmacological activities. Of particular interest, the inhibition was shown by both antitumor active and inactive glucans. These facts suggested that the recognition of beta-glucans by PM, which would proceed at a relatively early period of whole activation pathways, would not be enough to fully activate the host to show antitumor activity.

Animals↗
PubMed1995

Effects of the release of arachidonic acid from 1-ether-linked phospholipids on opsonized-zymosan stimulated rabbit alveolar macrophages.

On rabbit alveolar macrophages prelabeled with double tracers of [3H]arachidonic acid (20:4) for 30 min (short-term labeling) and of [14C]20:4 for 12 h (long-term labeling), the relationship between phospholipid subclasses and the release of 20:4 on stimulation with opsonized-zymosan (OZ) was investigated. Stimulation with 500 micrograms of OZ/ml for 1 h caused a significant decrease in the radioactivity of incorporated [3H]20:4 in all phosphatidylcholine (PC) subclasses of the cells: by 48% in 1-O-alkyl-2-acyl-sn-glycerol-3-phosphocholine (alkylacyl-GPC), and by 24% in 1,2-diacyl-GPC (diacyl-GPC), and slightly in 1-O-alk-1'-enyl-2-acyl-GPC (alkylacyl-GPC). In phosphatidylethanolamine (PE) a significant decrease in the incorporated [3H]20:4 was also observed in the 1,2-diacyl-sn-glycerol-3-phosphoethanolamine (diacyl-GPE, 45%). On the other hand, the radio activity of [14C]20:4 incorporated by long-term labeling into PC decreased significantly, by approximately 40%, in the alkylacyl-GPC and slightly in the alkenylacyl-GPC. In PE, a significant decrease (approximately 32%) in radioactivity of [14C]20:4 was observed only in the alkenylacyl-GPE which incorporated the largest amount of [14C]20:4 among the cellular phospholipids in its labeling and which showed the biggest decrease in [14C]20:4 in the PC and PE subclasses on stimulation with OZ. These results suggest that on OZ stimulation of rabbit alveolar macrophages, PC and PE subclasses involved in the mobilization of 20:4 depend on each 20:4 pool which is extracted in the cells.

Animals↗
PubMed2005

Dietary supplementation with n-3 polyunsaturated fatty acids attenuates the depression of food-motivated behavior during zymosan-induced peritonitis.

Peripheral inflammation is accompanied by neurobehavioral alterations such as depression of feeding, exploratory and sexual behaviors. Our previous investigation reported that dietary enrichment with n-3 polyunsaturated fatty acids (PUFA) attenuated the depression of food-motivated behavior and social exploration, but not endocrinological and metabolic disturbances in the mice with systemic inflammation induced by lipopolysaccharide (LPS). We here demonstrate that dietary n-3 PUFA also attenuate the reduction of food-motivated behavior during zymosan-induced peritonitis in mice without influencing plasma leakage into peritoneum and writhing response. Our results suggest that the common mechanism is involved in the attenuation of behavioral depression during systemic and local inflammation by dietary n-3 PUFA.

Animals↗
PubMed1989

Enhancement of zymosan-induced respiratory burst of rat neutrophils by lead in vitro.

The effect of Pb2+ on serum-treated zymosan (STZ)-induced O2 consumption of rat peritoneal neutrophils was studied. Pb2+ was found to mimic effectively the enhancing action of Ca2+ on the O2 consumption depending on the concentration up to about 80 microM. However, at concentrations over 80 microM, Pb2+ inhibited the O2 consumption. The enhancing effect of Pb2+ on the O2 consumption was further examined using the intracellularly Ca2(+)-depleted neutrophils. Pb2+ also enhanced the O2 consumption of the Ca2(+)-depleted cells as effectively as Ca2+. The Pb2(+)-enhanced O2 consumption of the Ca2(+)-depleted cells was inhibited by N-(6-aminohexyl)-5-chloro-1-naphthalene-sulfonamide (W-7) based on its calmodulin antagonistic action. The effect of Pb2+ on the activity of activator-deficient 3',5'-cyclic nucleotide phosphodiesterase (PDE), a calmodulin-dependent enzyme, was examined. Pb2+ activated PDE as effectively as Ca2+ only in the presence of calmodulin. The Pb2(+)-activated PDE activity was also inhibited by W-7 only in the presence of calmodulin. These results indicated that Pb2+ could replace Ca2+ in the activation process(es) of the respiratory burst, suggesting a possible involvement of calmodulin in the enhancing mechanism of the O2 consumption by Pb2+.

Animals↗
PubMed1980

Dissociated chemotactic responses to zymosan activated serum and bacterial chemotactic factor observed in a variety of diseases.

Chemotactic responses of patients with a variety of diseases to two different types of chemotactic factors were analyzed. Granulocytes were obtained from the patients with childhood malignant diseases during chemotherapy, the patients with measles, the adult patients with recurrent aphthous stomatitis, and newborn infants. 22 out of all the 38 patients (58%) showed decreased chemotactic response to zymosan activated human serum (ZAS), whereas only 9 patients (24%) showed decreased response to Escherichia coli-derived chemotactic factor (bacterial chemotactic factor: BCF). Furthermore, only 6 out of 22 patients who showed decreased chemotaxis to ZAS showed decreased chemotaxis to BCF. Analogous results were also obtained with cord blood granulocytes. These facts suggest that various kinds of chemotactic factors activate granulocytes in different ways, and that the evaluation of chemotactic response in a patient should be made simultaneously using more than two different types of chemotactic factor.

Adult↗
PubMed1989

Suppressive effect of 1-methyladenosine on the generation of chemiluminescence by mouse peritoneal macrophages stimulated with opsonized zymosan.

The preparation of an in vitro assay system for the immunosuppressive activities of modified nucleosides on macrophage (M phi) functions is described. Briefly, Listeria-elicited mouse peritoneal M phi s (Lm-M phi s) were treated with nucleosides in vitro for 18 hr at less than 1 mM concentration and chemiluminescence (CL) was measured after stimulation with opsonized zymosan. To confirm the usefulness of this assay (in vitro test), the immunosuppressive activities of 1-methyladenosine (m1 Ado) and adenosine (Ado) were determined by mouse Listeria infection (in vivo test), CL generation by M phi s obtained from the peritoneal cavity of nucleoside-treated mice (in vivo-in vitro test), and the in vitro test. The immunosuppressive activity of m1 Ado detected by the in vitro test was confirmed by the in vivo and the in vivo-in vitro tests. As for Ado, no immunosuppression was detected by the in vivo and the in vivo-in vitro tests through a potent suppressive effect was detected by the in vitro test. The ineffectiveness of Ado can be explained by the in vivo conversion of Ado to an inactive form. Thus, the proposed in vitro test seems to be useful, with the provision that the known in vivo metabolism is taken into consideration.

Adenosine↗
PubMed1984

Scanning electron microscopic analysis of Kupffer cell proliferation after zymosan administration.

Rat Kupffer cells were observed and counted under a scanning electron microscope after a single dose of zymosan. The cell number increased after 24 h and reached 2 times the control after 72 h. The percentage of cells presenting numerous microvilli increased from 24% to 86% over the same period. Carbon clearance, a measure of phagocytic activity, decreased temporarily, regained control values after 12 h, and attained a 4-fold elevation at 72 h. Phagocytic activity paralleled Kupffer cell number, but increased more relatively. This result probably reflected activation of resident Kupffer cells as noted by numerous thick microvilli.

Animals↗
PubMed1984

Inhibitory effect of nicotine on chemiluminescence response of human polymorphonuclear leukocytes stimulated by opsonized zymosan in vitro.

Effect of nicotine on chemiluminescence (CL) responses of human polymorphonuclear leukocytes (PMN) in vitro was investigated. Nicotine, ranging from 10(-5) to 5 X 10(-4)M, showed a concentration-dependent inhibition of the CL induced by 2.5 mg of opsonized zymosan. This inhibitory effect of nicotine (10(-4)M) on CL was not affected by atropine (10(-4)M), hexamethonium (10(-4)M) or acetyl beta-methylcholine (10(-4)M). These results indicate that nicotine directly acts to PMN with no relation of cholinergic affecting receptors. As to cytotoxic effects on PMN, assessed by the methods of trypan blue exclusion and of lactate dehydrogenase leakage from the cells, nicotine showed no cytotoxic effect on PMN in its range of 10(-5) to 5 X 10(-4)M. It is concluded that tobacco alkaloid nicotine could directly inhibit phagocytizing function of PMN. Furthermore, it is presumed that PMN circulating in the respiratory organs in tobacco smoking would be exposed to high concentrations of nicotine, and that the nicotine incorporated into the circulating system could suppress PMN functions resulting in harmful influences on the host defense mechanisms.

Cells, Cultured↗
PubMed1999

Selective regulation of cytokine induction by adenoviral gene transfer of IkappaBalpha into human macrophages: lipopolysaccharide-induced, but not zymosan-induced, proinflammatory cytokines are inhibited, but IL-10 is nuclear factor-kappaB independent.

Macrophages are the major cytokine producers in chronic inflammatory diseases, but the biochemical pathways regulating cytokine production are poorly understood. This is because genetic tools to dissect signaling pathways cannot be used in macrophages because of difficulties in transfection. We have developed an adenoviral technique to achieve high efficiency gene delivery into macrophages and recently showed that spontaneous TNF-alpha production in rheumatoid arthritis joint cells, chiefly from macrophages, is 75% blocked by adenoviral transfer of IkappaBalpha. In this report we use the same adenovirus to investigate whether the production of a number of proinflammatory cytokines (e.g., TNF-alpha, IL-1beta, IL-6, and IL-8) from human macrophages depends on NF-kappaB. While the cytokine response to certain inducers, such as LPS, PMA, and UV light, is blocked by overexpression of IkappaBalpha, the response to zymosan is not. In contrast, anti-inflammatory mediators (IL-10 and IL-1 receptor antagonist) induced by LPS are only marginally inhibited by IkappaBalpha excess. These studies demonstrate several new points about macrophage cytokine production. First, there is heterogeneity of mechanisms regulating both the proinflammatory and anti-inflammatory cytokines within populations of a single cell type. In addition, the results confirm the utility of the adenoviral technique for functional analysis of cytokine induction. The results also confirm that there are autocrine and paracrine interactions regulating cytokine synthesis within a single cell type. The selectivity of NF-kappaB blockade for proinflammatory but not anti-inflammatory mediators indicates that in macrophages, NF-kappaB may be a good target for the treatment of chronic inflammatory diseases.

Adenoviridae↗
PubMed2002

[Effects of periodontitis and opsonized zymosan on chemiluminescence of blood neutrophils].

The objective of the present investigation was to explore oxidative function of parodontitis patient's blood neutrophils stimulated with opsonized zymosan by method of luminol- and lucigenin-dependent chemiluminescence. The leukocytes for this study were obtained from peripheral venous blood of 16 parodontitis patients and 10 healthy subjects. The luminol-dependent chemiluminescence of stimulated neutrophils of parodontitis patients did not differ (p > 0.05) from control subjects (66,849 +/- 6372 cpm and 61,243 +/- 5240 cpm, respectively). Lucigenin-dependent chemiluminescence of stimulated neutrophils of parodontitis patients was increased (p < or = 0.001) comparing with control subjects (1361 +/- 169 cpm and 492 +/- 56 cpm respectively). The luminol- and lucigenin-dependent chemiluminescence (381 +/- 63 cpm, and 389 +/- 52 cpm, respectively) of nonstimulated neutrophils of parodontitis patients was significantly higher (p < or = 0.001) than analogous Cl (134 +/- 22 cpm and 138 +/- 16 cpm respectively) of control subjects. The results indicate that increased oxidative function of neutrophils of parodontitis patients possibly can affect parodontal health.

Adolescent↗
PubMed1992

Invertebrate cytokines II: release of interleukin-1-like molecules from tunicate hemocytes stimulated with zymosan.

Conditioned media and cell extracts from tunicate hemocytes that had been cultured with a variety of antigenic stimulants were tested for interleukin-1 (IL-1)-like activity. Media conditioned by hemocytes stimulated with zymosan significantly increased the proliferative and phagocytic activities of tunicate hemocytes. SDS-PAGE indicated that these biological activities were associated with the adaptive release of tunicate IL1-like (tunicate IL-1) molecules by stimulated hemocytes. The data suggest that tunicate IL1 molecules are expressed in response to selected antigenic stimuli. Such responses may form the basis for nonclonal, inducible immune reactions among phylogenetically primitive animals.

Animals↗