Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P43026 (lipopolysaccharide)
 62,215 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of Staphylococcus aureus enterotoxin A (SEA) and lipopolysaccharide (LPS) in cytokine production were assessed at the single cell level in cells obtained from healthy blood donors. Cytokine production was studied with UV-microscopy of fixed and permeabilized cells stained with cytokine specific monoclonal antibodies. The cytokines evaluated included tumour necrosis factor (TNF)-alpha, interleukin (IL)-1 alpha, IL-1 beta, IL-6, IL-8, IL-10, IL-2, IL-4, interferon (IFN)-gamma and TNF-beta. LPS exhibited marked production of IL-1 alpha, IL-1 beta, TNF-alpha, IL-6 and IL-8. After LPS stimulation IL-1 alpha, IL-1 beta, TNF-alpha and IL-8 were the dominating products, all peaking at or before 4 hours after cell stimulation. In addition, IL-10 production was evident after 12 hours of cell stimulation. The T-lymphocyte-derived cytokines TNF-beta, IL-2, IFN-gamma and IL-4 were never detected in the cultures. All cytokine production, except IL-8, was downregulated at 96 hours. In contrast, peak production of IL-1 alpha, IL-1 beta and IL-8, which were the dominant products, occurred after 12 hours in the SEA-stimulated cultures. Further, a significant T-lymphocyte production of TNF-beta, TNF-alpha, IFN-gamma and IL-2 was found with peak production 12-48 hours after initiation. Only low amounts of IL-6 were evident. The two types of cytokine pattern and kinetics found may correspond to the different clinical conditions after invasive Gram-negative Escherichia coli vs Gram-positive Staphylococcus aureus infections in humans, with a much more rapid onset of disease after E. coli infections.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Endotoxin and Staphylococcus aureus enterotoxin A induce different patterns of cytokines. 129 33

The epidemic form of the hemolytic uremic syndrome (HUS), beginning with an acute gastroenteritis, has been associated with a verocytotoxin-producing Escherichia coli infection. The endothelial cell is believed to play an important role in the pathogenesis of HUS. Endothelial cell damage by verocytotoxin-1 (VT-1) in vitro is potentiated by the additional exposure of inflammatory mediators, such as tumor necrosis factor-alpha (TNF-alpha). Preincubation of human umbilical vein endothelial cells (HUVEC) with TNF-alpha resulted in a 10- to 100-fold increase of specific binding sites for 125I-VT-1. Furthermore, interleukin-1 (IL-1), lymphotoxin (TNF-beta), and lipopolysaccharide (LPS) also markedly increase VT-1 binding. Several hours' exposure to TNF-alpha was enough to enhance the number of VT-1 receptors on the endothelial cells for 2 days. The TNF-alpha-induced increase in VT-1 binding could be inhibited by simultaneous addition of the protein synthesis inhibitor cycloheximide. Glycolipid extracts of TNF-alpha-treated cells tested on thin-layer chromatography demonstrated an increase of globotriaosylceramide (GbOse3cer), a functional receptor for VT-1, which suggests that preincubation of human endothelial cells with TNF-alpha leads to an increase in GbOse3cer synthesis in these cells. We conclude from this study that TNF-alpha and IL-1 induce one (or more) enzyme(s) that is (are) rate-limiting in the synthesis of the glycolipid VT-1 receptor, GbOse3cer. These in vitro studies suggest that, in addition to VT-1, inflammatory mediators play an important role in the pathogenesis of HUS.
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PMID:Tumor necrosis factor and interleukin-1 induce expression of the verocytotoxin receptor globotriaosylceramide on human endothelial cells: implications for the pathogenesis of the hemolytic uremic syndrome. 133

To test the importance of lipopolysaccharide (LPS) and adhesin as major antigens in vaccination against rabbit enteropathogenic Escherichia coli (EPEC)-like E. coli O103 infection, we used two nonpathogenic wild-type strains to immunize rabbits at weaning. One of these strains (C127) harbors the O103 LPS but does not express the 32,000-molecular-weight adhesin that characterizes the highly pathogenic O103 strains. The other (C6) belongs to the O128 serogroup, which does not cross-react with the O103 serogroup, but expresses the adhesin. These strains were administered orally, either live or after Formalin inactivation. After vaccination, the animals were challenged with highly pathogenic O103 strain B10. Compared with rabbits vaccinated with the Formalin-killed homologous strain, rabbits vaccinated with killed C127 or C6 showed partial but significant protection. When given live, these strains colonized more or less heavily the digestive tract of the animals and provided nearly complete (C127) or complete (C6) protection against challenge. They induced a quick local immune response, as judged by fecal immunoglobulin A anti-LPS kinetics. Furthermore, strain C6 induced an ecological effect of "resistance to colonization" against challenge strain B10. This effect may have been due to the adhesin that is shared by both strains and to the production of a colicin. Strain C6 could inhibit in vitro the growth of highly pathogenic O103 strains. On the whole, our results show that adhesins and LPS are important, although probably not exclusive, protection-inducing components in rabbit EPEC-like colibacillosis and provide insight into possible protection of rabbits against EPEC-like E. coli infection with live strains.
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PMID:Oral vaccination of weaned rabbits against enteropathogenic Escherichia coli-like E. coli O103 infection: use of heterologous strains harboring lipopolysaccharide or adhesin of pathogenic strains. 135 80

Fifteen and five of 20 volunteers challenged with the enterotoxigenic Escherichia coli strain O 78.H11 showed a fourfold titre increase of serum ELISA antibody to the homologous O 78 and the heterologous O 8 lipopolysaccharide antigen, respectively. Sixty-three of 191 sera from 1- to 48-month-old German children showed serum antibody reactive with O 78 antigen, all but two of these O 78-positive sera also showed reactivity with at least one further O antigen. Only 14 of the O 78 reactive sera also showed antibody to heat-labile enterotoxin. In addition, soluble O 8 antigen could inhibit the binding of serum antibody to absorbed O 78 in 68% of the German children. Antibody reactive with O 78 antigen is thus not a reliable serological marker for enterotoxigenic E. coli infection in German children.
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PMID:Reactivity of human serum antibody with lipopolysaccharide O 78 antigen from enterotoxigenic Escherichia coli. 137 19

Acyloxyacyl hydrolase (AOAH), an enzyme that removes the secondary acyl chains of gram-negative bacterial lipid A (endotoxin), has been identified previously in human neutrophils and mouse macrophages. We report here that bovine leukocytes also contain AOAH activity. Although bovine AOAH deacylates bacterial lipopolysaccharide in a manner similar to human AOAH, it is active in vitro over a broader pH range, from 4.0 to 7.0. By using Escherichia coli infection of the bovine mammary gland as a model of localized gram-negative bacterial disease and associated tissue inflammation, AOAH activity per leukocyte increased. In addition, AOAH activity increased in the cell-free portion of infected mammary secretions. These data indicate that AOAH activity increases in leukocytes associated with inflammation induced by gram-negative bacteria and provide additional evidence of its potential involvement in the defense against the effects of bacterial endotoxin.
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PMID:Intracellular and extracellular enzymatic deacylation of bacterial endotoxin during localized inflammation induced by Escherichia coli. 198 68

Mouse hybridoma antibodies (IgG and IgM) to O side chain determinants of Escherichia coli strain Bort (O18ac:K1:H7) were evaluated for their in vitro and in vivo activities against E. coli strains. Both IgG and IgM were opsonic in vitro and protected newborn rats challenged with a K1 E. coli strain, but their activities were strain specific. The antibodies protected against a K1 strain possessing a homologous O serotype but not against one possessing a heterologous O serotype. These antibodies were not effective against the K5-encapsulated O18 E. coli strain (possessing a homologous O type) but protected against its unencapsulated derivative. The opsonic and protective activities of these antibodies were significantly greater with IgG than IgM. Both IgG and IgM, however, required complement for their activities. When IgM to lipopolysaccharide was given to newborn rats in conjunction with IgM monoclonal antibody to the group B meningococcal polysaccharide, the protective effect was significantly greater than that of either antibody alone. Combinations of two (or more) antibodies to different cell wall components may be more beneficial in preventing and treating E. coli infection.
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PMID:Functional activities of monoclonal antibodies to the O side chain of Escherichia coli lipopolysaccharides in vitro and in vivo. 244 99

The serum antibody response of patients infected with alpha-hemolysin (AH)-producing Escherichia coli was measured by three immunoassays: tube neutralization, microneutralization, and enzyme-linked immunosorbent assay. All three assay results showed good correlation with each other. The mean anti-AH titer in patients with E. coli infection was higher than the mean titer in noninfected patients. The hemolysin-neutralizing activity was immunoglobulin G. The amount of lipopolysaccharide (LPS) antibody did not correlate with the amount of AH antibody. LPS antibody measured by enzyme-linked immunosorbent assay was predominantly of the immunoglobulin G class. Adsorption of LPS antibody by E. coli H79 LPS did not affect anti-AH titers, indicating that LPS and AH have different antigenic determinants. AHs prepared from several different E. coli strains had identical or similar antigenic determinants at the active site. Hemolysin proteins separated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis were stained identically by human sera with AH antibody and by a mouse monoclonal AH antibody.
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PMID:Immune response to Escherichia coli alpha-hemolysin in patients. 245 38

An experimental Escherichia coli septicaemia-peritonitis model was adapted to immunosuppressed mice. The mice were made neutropenic by a sublethal dose of cyclophosphamide, which resulted in a 100-fold increase in their susceptibility to intraperitoneal injection of E. coli O18:K1. A lethal infection could be prevented by passive immunisation with anti-K1 capsular or anti-O18 LPS antibodies but not with anti-J5 bacterial antibodies. The anti-K1 and anti-O18 antisera were able to increase the LD50 of the E. coli challenge by factors of 50 and 5, respectively. The role of non-specific, lipopolysaccharide (LPS)-mediated resistance to infection was also investigated in this model, in which only long-living phagocytic cells such as macrophages are believed to be functional. Pretreatment of mice with LPS was shown to prevent growth of the bacterial challenge in the peritoneal cavity and blood and to result in a five-fold increase in the LD50 of the challenge strain. These findings suggest an important role for macrophages as effector cells in defence against E. coli infection.
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PMID:Experimental Escherichia coli peritonitis in immunosuppressed mice: the role of specific and non-specific immunity. 327 82

A high degree of non-specific resistance to a lethal systemic Escherichia coli infection was induced in mice by pretreatment with a small dose (less than 5 micrograms/mouse) of the homologous lipopolysaccharide (LPS) or with heterologous rough-type LPS from E. coli K-12. The route of LPS administration, intraperitoneally or subcutaneously, did not influence the development of resistance, suggesting that a systemic cell activation was responsible for the effect. The enhanced elimination of bacteria was similar to that in mice recovering from a sublethal E. coli infection. In the LPS-treated mice, elimination of the challenge bacteria from the peritoneal cavity and the blood started 3-4 h after challenge whereas, in controls, the bacterial numbers continued to increase until the mice died. The detoxified LPS derivative, monophosphoryl lipid A (MPL), also increased the survival of mice infected with E. coli O18:K1. However, the dose of MPL required for optimal infection resistance was 100-fold greater than that of native, E. coli K-12 LPS, corresponding to the 100-fold reduced toxicity of MPL for mice and rabbits in lethality and pyrogenicity assays.
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PMID:Lipopolysaccharide-induced non-specific resistance to systemic Escherichia coli infection in mice. 327 15

The contribution of activated macrophages to protection against Escherichia coli was studied in mice treated intravenously with Corynebacterium parvum 7 days before infection. C. parvum-treated mice showed increased phagocytic activity and enhanced resistance to Listeria infection. In contrast, these mice showed increased susceptibility to a subsequent challenge with E. coli that correlated closely with a reduction in the LD50 of lipopolysaccharide (LPS) in these mice. The peritoneal macrophages obtained from C. parvum-treated mice had a strong ability to phagocytize and kill E. coli in in vitro experiments. A rapid decline in the number of bacteria in the liver of C. parvum-treated mice was observed in the early period of infection. However, the number of bacteria in liver and spleen increased progressively to a lethal dose from 6 hr after infection. At this time, a significant increase in beta-glucuronidase, a lysosomal acid hydrolase, was found in the serum of these mice. In vitro experiments revealed that the peritoneal macrophages from C. parvum-treated mice were highly susceptible to the cytotoxic effect of LPS after 6 hr of incubation with LPS. It is suggested that the hypersensitivity of activated macrophages to the cytotoxic effect of endotoxin derived from E. coli may be partly responsible for the increased susceptibility of C. parvum-treated mice to E. coli infection.
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PMID:Increased susceptibility to Escherichia coli infection in mice pretreated with Corynebacterium parvum. 634 89


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