SEARCH · PubMed Health
Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
The comparative studied on lipopolysaccharides from Yersinia pseudotuberculosis IVA serovar, strains 32 and 31D, have been conducted. The identity of the lipopolysaccharides isolated from these strains has been shown. The structural pattern of the repeating unit of the O-specific side chain of the lipopolysaccharide has been suggested: (Formula: see text)
In vaccines consisting of acetone-killed Salmonella, 90% of the bacteria were replaced by: heterologous Salmonella S-forms, R-mutants of Salmonella or Escherichia coli, lipopolysaccharide from S. typhimurium (S-form) or from R-mutants of Salmonella or E. coli and by muramyl dipeptide. Active immunizations of NMRI mice with these vaccines were undertaken. Mice received two intraperitoneal injections of the vaccines at intervals of 14 days, and were challenged with various doses of S. typhimurium C5 10 days later. The protective capacity of the mixed vaccines was compared with that of monovaccines (S. typhimurium) and with the effectiveness of vaccines consisting of the supplementing component (relatively weak immunizing ability) alone. The LD50 served as criterion for protective capacity. The results showed that S. typhimurium S-form could be replaced by Salmonella R-mutants belonging to different chemotypes without a recognizable decrease in protective immunizing capacity of the vaccines. Effective vaccines were also attained when heterologous Salmonella S-forms, which exhibit no O-antigenic determinants in common with S. typhimurium, were used as supplements. Mixtures with E. coli R-mutants proved to be less effective. In addition, the diminished dose of S. typhimurium could be so effectively supplemented with lipopolysaccharide from S. minnesota R 595 that complete protection was achieved. In contrast, comparable doses of R lipopolysaccharides from E. coli were somewhat less effective. Vaccines of LPS-extracted bacteria exhibited a reduced protective capacity and were ineffective when used as supplements in mixed vaccines. Analogous results were obtained when R-mutants served as basic vaccines in place of the S. typhimurium S-form indicating that an immunogenic component is enhanced in these organisms too and that their immunogenic capacity is not brought about barely by general stimulation of the immune system. However, the full effectiveness of the R-monovaccines was often not attained with supplements. Immunization with mixed vaccines of S. typhimurium S-form and heterologous Salmonella S-forms or Salmonella R-mutants led to equally high agglutinin and haemagglutinin titers as those obtained with monovaccines of S. typhimurium S-form.
Alkali-treated lipopolysaccharides of a range of enterobacterial R mutants with complete and incomplete core structures were investigated by agar gel and microcapillary precipitation onto their reactivity with three selected commercial lectins, namely Concanavalin A, Ricinus communis agglutinin and Wheat germ agglutinin. R lipopolysaccharides with complete R cores of the six so far established core types were differentiable from each other by their characteristic lectin reactivity pattern. One core type showed no reaction with all the three lectins. R lipopolysaccharides with incomplete core structure showed in general the reactivity pattern predictable from their individual chemical configuration. It was further shown that substitution of complete R cores by haptens (T1, T2 or ECA) or by a single repeating unit (SR mutant) did not change the reactivity pattern, although some interactions were less pronounced. It will be demonstrated that lectin precipitation can be of help for structural studies in recognizing, for example, terminal sugar units and their anomeric linkages.
Examination of the mitogenic response of lymphocytes in 50 blood samples from 17 patients suffering from Pseudomonas aeruginosa infection and on 5 occasions from 5 healthy persons revealed that a Pseudomonas lipopolysaccharide unfamiliar to the lymphocytes decreased, whereas the purified O-antigen of the infection causing Pseudomonas serogroup increased the effect of phytohaemagglutinin on parallel lymphocyte cultures prepared from the same blood samples during the whole infectious process. After complete recovery, however, the lipopolysaccharide of the infection causing P. aeruginosa strain inhibited again the phytohaemagglutinin response as if the lymphocytes had never met it. The model seems to offer a possibility to follow up in vivo the signs of the changes in the cellular background during the reaction given on Pseudomonas lipopolysaccharides.
Two amidases have been partially purified from the slime mold Dictyostelium discoideum; these act sequentially on the beta-hydroxymyristyl-amide groups present in the lipopolysaccharide derivative (4'-O-phosphoryl-N-beta-hydroxymyristyl-D-glucosaminyl)-beta-(1 leads to 6)-N-beta-hydroxymyristyl-D-glucosamine-1-phosphate (III). Amidase-I, which specifically removes the myristyl chain near the 1-phosphate of compound III (apparent Km, 3.7 microM), has been purified 110-fold from a lysate of D. discoideum NC4 cultivated on Escherichia coli. The partially purified enzyme contains no other amidase or phosphatase activities; however, an esterase activity can be detected. The second amidase has been purified about 12-fold from the extracellular fluid of D. discoideum AX3 cultured axenically. This amidase hydrolyzes the distal amide linkage in III (apparent Km, approximately 20 microM) only after prior deacylation of the first site by amidase-I. The preparation is free from phosphatases and glycosidases that can act on lipopolysaccharide. The differential expression of the amidases in D. discoideum and some of their kinetic properties have been described. The amidases should prove useful in structure-function studies of lipopolysaccharide.
A gastric mucosal mucin receptor has been isolated from the epithelial cell membrane by affinity chromatography on wheat germ agglutinin. The receptor protein displayed an apparent molecular weight of 97kDa and exhibited binding specific to gastric mucin in a concentration-dependent manner. The binding of mucin to the mucosal receptor was inhibited by lipopolysaccharide from H. pylori. The inhibitory effect was proportional to the concentration of lipopolysaccharide up to 30 micrograms/ml, at which concentration a 91% decrease in binding occurred. The results suggest that H. pylori lipopolysaccharide is capable of disrupting the integrity of mucus perimeter of gastric mucosal defense by interfering with epithelial cell-mucin binding.
A gastric mucosal somatostatin receptor was isolated from the solubilized epithelial cell membrane by affinity chromatography on a column consisting of covalently coupled [D-Tryp8]SRIF-14 to Affi-Gel 10. The receptor protein displayed a molecular weight of 61kDa and exhibited specific affinity towards 125I-labeled [Tyr11]SRIF-14 with the optimum range of 4-8 micrograms/ml. The binding of somatostatin to its mucosal receptor was inhibited by lipopolysaccharide from H. pylori. The inhibitory effect was proportional to the concentration of lipopolysaccharide up to 50 micrograms/ml and reached a maximum of 94.1% inhibition. The results suggest that H. pylori, through its lipopolysaccharide, is capable of interfering with somatostatin regulatory effect on gastric mucosal G-cell function.
The effect of paraformaldehyde-fixed murine macrophage P388D1 cells stimulated with Actinobacillus actinomycetemcomitans Y4 lipopolysaccharide (membrane-associated interleukin-1) on osteoclastic bone resorption was investigated. Both the number of osteoclasts and the bone resorption surfaces increased considerably along the inside of the marrow space of mouse calvaria when membrane-associated interleukin-1 mediated by A. actinomycetemcomitans Y4 lipopolysaccharide were injected into the subcutaneous tissues overlying the central calvaria of 4-week-old C3H/HeJ mice. Membrane-associated interleukin-1 caused hypercalcaemia when injected into C3H/HeJ mice twice a day for 2 days. The calvaria of C3H-HeJ mice injected with membrane-associated interleukin-1 contained less mineral than those of the control mice. These results suggest that membrane-associated interleukin-1 on macrophages stimulated with A. actinomycetemcomitans Y4 lipopolysaccharide plays an important role in inflammatory osteoclastic bone resorption in periodontal diseases.
The F6R rough mutants isolated from Shigella flexneri F6S, serotype 5b, and the FH rough mutants, derived from other serotypes of S. flexneri, were chemotyped according to the chemical analysis of their lipopolysaccharides. Further, the following stages of lipopolysaccharide core biosynthesis in S. flexneri have been established: --(KDO)3--heptose--heptose--glucose--galactose; the last three stages are: either --glucose--glucosamine--glucose, or --glucosamine--glucose--glucose. The results of the chemical study of the R lipopolysaccharides are compatible with the assumption of the existence of a similar core in all considered S. flexneri serotypes.
The effect of methylprednisolone on superoxide production by pulmonary and circulating blood neutrophils was investigated in rats after the intravenous injection of lipopolysaccharide. Superoxide production by both types of neutrophils was increased by lipopolysaccharide injection, and pretreatment with methylprednisolone inhibited this increase. The inhibitory effect of methylprednisolone on pulmonary neutrophils was greater than that on circulating blood neutrophils. Methylprednisolone also prevented the increase in pulmonary vascular permeability induced by lipopolysaccharide, but failed to inhibit intrapulmonary neutrophil accumulation. These results suggest that the suppression of superoxide production may be one mechanism by which methylprednisolone prevents endotoxin-induced lung damage.
Seven bacteriophages specifically lytic for representative strains of Shigella flexneri serotype 6 were studied. Cross hemagglutination experiments and chemical analysis of isolated lipopolysaccharides showed that strains 975 and 323 are smooth and strains 288, 551 and 488--rough. Lipopolysaccharides isolated from the smooth strains inactivated phages F10 and "a" whereas those from the rough strains demonstrated poor inactivation of specific bacteriophages. The lipopolysaccharides of both the smooth and rough strains were found to be phage "a" receptors. The results indicate that the varied sensitivity of S. flexneri 6 depends on the roughness of the strains.
A preferential cell mediated response is obtained after stimulation with oxazolone () and a humoral response is seen after E. coli lipopolysaccharide (LPS) immunization (). Thus a cytological study of selectively isolated antigen recognizing cells which form rosettes and antibody producing cells which form hemolytic plages has been performed during oxazolone and lipopolysaccharide stimulations. This investigation shows quantitative and qualitative differences of these immunocyte subpopulations in the two stimulations. First the antigen recognizing cells antibody producing cells ratio is fundamentally much higher at all the stages of the oxazolone stimulation than after lipopolysaccharide immunization. On the other hand among these immunocyte subpopulations, T and B cells are identified by electron microscopy in the oxazolone immune reaction, while only B cells are observed after LPS immunization.
In liver grafts that will fail as a result of storage injury, reperfusion activates Kupffer cells. Overproduction of tumor necrosis factor by activated Kupffer cells may cause primary graft nonfunction, multiple organ failure and, eventually, death of graft recipients. Carolina rinse solution, adenosine, nisoldipine, pentoxifylline and prostaglandin E1 reduce graft failure from storage/reperfusion injury. To test the hypothesis that these agents act by suppressing cytokine release by activated Kupffer cells, we assessed the effect of each drug on tumor necrosis factor released from cultured rat Kupffer cells stimulated with lipopolysaccharide. Adenosine, nisoldipine and prostaglandin E1 each suppressed lipopolysaccharide-stimulated tumor necrosis factor release. The adenosine A2 receptor agonists. 5-n-ethylcarboxamidadenosine, 2-chloro-adenosine and R-phenylisopropyl adenosine also blocked tumor necrosis factor release in a potency suggestive of A2 receptor activity. Xanthine amine congener, a specific A1 receptor antagonist, failed to reverse the suppression by adenosine of tumor necrosis factor release, whereas CGS15943A, an A2 receptor antagonist, did reverse suppression by adenosine and 5-n-ethylcarboxamidadenosine. CGS15943A had no effect on suppression of lipopolysaccharide-stimulated tumor necrosis factor release by nisoldipine or prostaglandin E1. Dibutyryl-cyclicAMP also suppressed tumor necrosis factor release. Adenosine, 5-n-ethylcarboxamidadenosine, prostaglandin E1 and pentoxifylline increased cyclicAMP levels in cultured Kupffer cells, but nisoldipine did not.(ABSTRACT TRUNCATED AT 250 WORDS)
Tissue factor, the cellular receptor for factor VII/VIIa, activates both the intrinsic and extrinsic pathways of blood coagulation. In this analysis we have used DNase I footprinting to map the sites of protein-DNA interaction along the promoter (-383 to +8) using nuclear extracts prepared from uninduced and lipopolysaccharide-induced THP-1 cells. We have identified six regions that interact with nuclear factors in both uninduced and induced extracts. Four footprints are contained within a region reported to confer base-line high level expression and lipopolysaccharide and serum induction. Two additional footprints map to a region reported to reduce basal transcription by 50%. The only qualitative change in the footprint pattern with uninduced and induced extracts is the appearance of two hypersensitive sites with uninduced extracts. In addition, changes in the level of protein- DNA binding are detected with only one probe by DNA mobility shift analysis. A combination of well characterized transcription factors (AP1), primarily lymphoid cell specific regulatory proteins (NF-kappa B- and/or Ets-1-related proteins), as well as additional, uncharacterized proteins appear to interact with these sequences. Our data suggest that post-translational modification of existing transcription factors, and not induction of new DNA-binding activity, mediates the lipopolysaccharide induction of tissue factor synthesis in THP-1 cells.
The effect of intracerebroventricular (icv) administration of lipopolysaccharide on histidine decarboxylase activity and histamine content in the hypothalamus were investigated in male mice of ddY strain in vivo. Two-fold increase in histidine decarboxylase activity (HDC) was observed 4 h after administration of 50 mcg lipopolysaccharide, and HDC activity returned to the basal level within 12 h after injection. Furthermore, histamine contents showed a slight decrease at 1 and 2 h and a mild increase at 12 h after administration. However, changes in histamine content were not statistically significant. These results suggest that the increase of HDC activity in the hypothalamus by lipopolysaccharide may be involved in the central neuroimmune responses.
Lipopolysaccharide from phenol-water extraction of cells of Campylobacter coli serotype O:30 was separated as a water-insoluble gel of low M(r) from a water-soluble antigenic polysaccharide of high M(r). Acetic acid hydrolysis of the ketosidic linkages to lipid A in the lipopolysaccharide furnished a core oligosaccharide. Structural investigations were performed using 1H and 13C NMR, fast atom bombardment-mass spectrometry of permethylated derivatives, and methylation linkage analysis on the core oligosaccharide and the products of two successive Smith degradations. It is concluded that the highly branched 3-deoxy-D-manno-octulosonic acid-terminated oligosaccharide chains carried at the nonreducing end disaccharide units of beta-D-Qui3NAc-(1-->2)-beta-D-Qui3NAc (where Qui3NAc represents 3-acylamino-3,6-dideoxy-D-glucose), in which N-acyl residues were either both (R)-3-hydroxybutanoyl or both 3-hydroxy-2,3-dimethyl-5-oxoprolyl. The demonstration of these unusual features provides further evidence for a wide variety of structures within the core oligosaccharide region of lipopolysaccharides from Campylobacter sp.
Immunochemical studies on Shigella sonnei and serotype 6 Shigella flexneri 0 antigens (lipopolysaccharides) and enterobacterial common antigen (ECA) isolated from Shigella sonnei were carried out. Oligosaccharide structure of 0-specific chain of serotype 6 Shigella fiexneri lipopolysaccharide was defined and beta-L-rhamnosyl-1,3-N-acetyl-D-galactosamin as immunodeterminant of type VI specificity was recognized. The structures of core regions of lipopolysaccharides isolated from R mutants of both Shigella subgroups were established. On the base of the serological and structural results it has been suggested that these core regions are identical and very close to RI core structure of E. coli C. The effective method of isolation and purification of enterobacterial common antigen from Shigella sonnei was elaborated and its immunological properties as well as chemical character defined.
OBJECTIVE: To investigate the effects of anti-inflammatory drugs on lipopolysaccharide-induced procoagulant activity of bovine alveolar macrophages. DESIGN: Procoagulant activity was induced in bovine alveolar macrophages from 4 healthy Holstein calves aged 6 to 16 weeks by incubation with lipopolysaccharide. 3 anti-inflammatory drugs were used at 4 concentrations and 3 times to pretreat the alveolar macrophages. Results were analyzed to determine whether drug, concentration, or exposure period had a significant (P > 0.05) effect. PROCEDURE: Bovine alveolar macrophages, harvested by volume-controlled bronchoalveolar lavage, were pretreated for 30, 60, or 120 minutes with an anti-inflammatory compound (dexamethasone, flunixin meglumine, or phenylbutazone) at several concentrations ( 0, 1, 10, and 100 microM). Bovine alveolar macrophages were exposed to lipopolysaccharide (Escherichia coli O55:B5) in the presence and absence of fetal bovine serum for 4 hours. Procoagulant activity was measured, using a chromogenic assay. RESULTS: None of the drugs was associated with a modification of procoagulant activity expression. CONCLUSION: Use of these 3 anti-inflammatory drugs is unlikely to modify the extent of the fibrinous reaction commonly observed in cases of acute bovine respiratory tract disease complex. CLINICAL RELEVANCE: The alveolar macrophage has a key role in fibrin production. Assuming in vivo events mimic the in vitro model, is appears unlikely that administration of anti-inflammatory drugs will reduce the procoagulant activity of the bovine alveolar macrophages and the directly associated pulmonary fibrosis.