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)

Certain strains of verotoxigenic Escherichia coli (VTEC), and in particular those belonging to serogroup O157, cause attaching and effacing (AE) lesions of the host gut mucosa during pathogenesis. The mechanisms involved with bacterial attachment and the destruction of microvilli are determined by a cluster of genes within the LEE region, which also encode five secreted proteins. Sera from patients with antibodies to the lipopolysaccharide (LPS) of E. coli O157 and other VTEC were tested for antibodies to these secreted proteins. Twenty-one of 34 (62%) sera with antibodies to the lipopolysaccharide (LPS) of E. coli O157 also contained antibodies to one or more of the secreted proteins. Five of 12 sera containing antibodies to the LPS of a range of other VTEC serogroups also contained antibodies to 1 or more of the 5 secreted proteins, as did 16 of 70 (23%) sera from patients with haemolytic uraemic syndrome (HUS), haemorrhagic colitis (HC) or diarrhoea, but without bacteriological evidence of infection with VTEC and which did not contain antibodies to VTEC serogroups O5, O115, O145, O153 or O157. The detection of serum antibodies to secreted proteins may provide additional information for interpreting the results of established lipopolysaccharide-based VTEC serology.
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PMID:Serum antibodies to secreted proteins in patients infected with Escherichia coli O157 and other VTEC. 969 1

We report the case of an Escherichia coli O157:H7 infection in a patient with hemorrhagic colitis. Initial diagnosis was ischemic colitis because of the age of the patient and clinical presentation. After one week, a hemolytic-uremic syndrome occurred and serologic antibodies to the lipopolysaccharide O157 of Escherichia coli O157:H7 were positive, leading to the diagnosis of hemorrhagic colitis caused by this bacteria. Escherichia coli O157:H7 colonic infection is not well known, specially in France where only two cases has been reported in adults. This bacteria and the toxin produced (Shiga-like toxin) should be searched in cultures of stools and colonic biopsies in case of bloody diarrhea, in particular when a hemolytic-uremic syndrome is associated. As clinical, pathological and endoscopic findings in Escherichia coli O157:H7-associated colitis may be similar to the ischemic colitis pattern, differential diagnosis may be difficult.
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PMID:[Hemorrhagic colitis and hemolytic uremic syndrome caused by Escherichia coli O157:H7]. 979 63

Proinflammatory cytokines are believed to be involved in the pathogenesis of ulcerative colitis (UC). The aim of this study was to clarify the profiles of proinflammatory cytokine production in patients with UC in terms of disease intractability, endoscopic findings, and host response to lipopolysaccharide (LPS) stimulation. Colonic mucosal tissues were obtained from patients with active UC (n = 15, including 4 patients with intractable disease) and inactive UC (n = 7), non-inflammatory bowel disease (IBD) colitis (n = 11), and controls (n = 20). Organ culture was performed, and the amounts of four cytokines (described below) in the culture media were determined by enzyme-linked immunosorbent assay (ELISA). LPS stimulation enhanced interleukin (IL)-1beta, IL-8, and IL-6 production in colonic specimens from all groups, but enhanced tumor necrosis factor (TNF)-alpha production only in active UC specimens. Levels of IL-6, IL-8, and TNF-alpha were significantly higher in active UC than in non-IBD colitis, and the production of all three of these cytokines was correlated to the endoscopic grade of inflammation. The production of these cytokines was also significantly higher in patients with intractable disease receiving corticosteroids than in patients with non-intractable disease receiving corticosteroids. These results suggest that enhanced production of mucosal proinflammatory cytokines may be implicated in the pathogenesis of UC.
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PMID:Mucosal proinflammatory cytokine production correlates with endoscopic activity of ulcerative colitis. 1020 29

It has been suggested the the interaction of Escherichia coli O157-derived verotoxins (VTs) with the vascular endothelium plays a central role in the pathogenesis of the thrombotic microangiopathy and ischemic lesions characteristic of hemolytic uremic syndrome (HUS) and E. coli O157-associated hemorrhagic colitis. Intravenous administration of both E. coli O157-derived VT1 and lipopolysaccharide (LPS) in the rat induced a synergistic increase in thiobarbituric acid (TBA) values in those animal's plasma, as compared with that injected with VT1 or LPS alone. We then hypothesized that an increase in lipid peroxidation in the rat plasma was due to an enhanced production of endothelial cell-derived reactive oxidant. Based on determination of rat sera and cultured human aortic endothelial cells (HAECs), VT1 had little if any effect on LPS-stimulated increase of nitric oxide and the resultant peroxynitrite generations. Both RT-PCR and Western blot studies of reactive oxygen species-related enzymes showed that VT1 markedly decreased the expression of catalase mRNA and protein in HAECs, but caused less alteration in the levels of Cu, Zn-superoxide dismutase, and NADPH oxidase mRNA. Further studies by spin trapping analysis using 5, 5-dimethyl-1-pyrroline-N-oxide (DMPO) revealed a time-dependent increase in hydroxyl radicals by VT1 in HAECs. The accumulated data thus suggest that bacterial VT1 reduces mainly catalase levels in endothelial cells, which is synergistically potentiated by LPS, and that the resulting hydroxyl radical participates in endothelium injury through a marked enhancement of lipid peroxidation, leading to HUS.
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PMID:Reactive oxygen species as a risk factor in verotoxin-1-exposed rats. 1040 47

We developed the enzyme-linked immunosorbent assay (ELISA) for detection of serum IgM and IgG antibodies to lipopolysaccharide (LPS) of Escherichia coli O157:H7 (VT1+, VT2+) isolated from a clinical sample. We tested the patient's sample with hemolytic uremic syndrome (HUS) and hemorrhagic colitis (HC). And we evaluated the value of sample OD to cut off control OD as the Index. The CVs obtained in precision studies were below 10% for intra- and inter-assay, respectively. The cut off index value of infants and children (0 to 5 years) was 0.60 for IgM and 0.95 for IgG. Moreover we investigated the specificity to E. coli O157 from other E. coli serotypes in this method. From these results, O27 serotype was crossreacted in this assay, but other serotypes were not reacted. In the patients with HUS and HC, some cases were already positive for IgM at 3 days, but for IgG 8 days were needed for it to become positive. We concluded that this ELISA for IgM and IgG for E. coli O157 LPS have a useful performance, and might be the useful tool for rapid diagnosis for E. coli O157 infection.
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PMID:[Development of an enzyme-linked immunosorbent assay (ELISA) for detection of IgM and IgG antibodies to lipopolysaccharide of Escherichia coli O157]. 1042 50

IL-12 modulates Th1 immune response during chronic colitis. Mechanisms regulating IL-12 synthesis in human intestine are poorly understood. The aim of this study was to investigate the effect of IFN-gamma and PGE2 on lipopolysaccharide (LPS)-stimulated LPMC IL-12 production. Normal LPMC cultures were run in the presence or absence of IFN-gamma and/or PGE2 before LPS stimulation. To examine the role of endogenous PGE2 on LPS-stimulated IL-12 release, LPMC cultures were added of indomethacin before LPS stimulation. IL-12, IL-10 and IL-8 were measured by ELISA. No IL-12 was detected in either unstimulated or LPS-stimulated LPMC cultures. In contrast, LPMC released IL-8 (650 +/- 125 pg/ml) and IL-10 (75 +/- 25 pg/ml) in response to LPS. Treatment of LPMC with IFN-gamma facilitated LPS-stimulated IL-12, whereas it completely abrogated IL-10 production. IL-12 release by LPMC stimulated with IFN-gamma and LPS was significantly inhibited by exogenous IL-10. The addition of PGE2 to IFN-gamma-treated LPMC cultures inhibited in a dose-dependent manner LPS-induced IL-12 secretion. Furthermore, IL-12 was detectable (85 +/- 25 pg/ml) in the supernatants of LPMC cultures treated with indomethacin and LPS. In contrast to the effect on IL-12, PGE2 significantly augmented LPS-stimulated LPMC IL-10 production. However, the inhibition of IL-12 by PGE2 was only partially reversed by anti-IL-10. In a simplified model of LPS tolerance, we finally showed that monocyte-derived macrophages exhibited reduced IL-12 production after repeat LPS stimulation. In these cell cultures, indomethacin abrogated the induction of LPS desensitization. IFN-gamma and PGE2 modulate differently the LPMC responsiveness to LPS in terms of IL-12 synthesis.
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PMID:Interferon-gamma (IFN-gamma) and prostaglandin E2 (PGE2) regulate differently IL-12 production in human intestinal lamina propria mononuclear cells (LPMC). 1046 49

In acute DSS-induced colitis nuclear factor (NF)-kappaB-dependent inflammatory cytokines including IL-1 and tumour necrosis factor-alpha (TNF-alpha) are up-regulated. Here we examined the effects of gliotoxin, a fungal metabolite known to inhibit NF-kappaB activity, on cytokine production by a mouse cell system in vitro and on intestinal inflammation and NF-kappaB activation in vivo. In vitro gliotoxin decreased TNF-alpha gene expression and protein production by RAW-264.7 mouse macrophage-like cells stimulated with lipopolysaccharide. In vivo, gliotoxin treatment of mice was begun on day 3 of 5% DSS application dissolved in the drinking water and continued until day 8. Gliotoxin treatment dose-dependently down-regulated colonic inflammation as assessed histologically and in parallel there was a suppression of colonic TNF-alpha and IL-1alpha mRNA expression on day 8 as analysed by semiquantitative reverse transcriptase-polymerase chain reaction (P < 0.01). Furthermore, colonic NF-kappaB DNA-binding activity was increased in DSS-induced colitis and was suppressed by gliotoxin. These results demonstrate the essential role of NF-kappaB in DSS-induced colitis and indicate a molecular approach to the treatment of intestinal inflammatory disorders.
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PMID:Nuclear factor-kappa B activity and intestinal inflammation in dextran sulphate sodium (DSS)-induced colitis in mice is suppressed by gliotoxin. 1075 64

Berberine is an isoquinoline alkaloid with multiple pharmacological actions, including anti-inflammatory activity. The aims of this study were to examine the effect of berberine on the mucosal healing process and to investigate whether berberine can inhibit the increased production of interleukin-8 in trinitrobenzene sulfonic acid-induced colitis in rats. Berberine was administered orally for 3 days or 1 week at a dosage of 7.5 or 15 mg/kg/day. Tissue damage scores, body weight, colon wet weight, and colon wall thickness were measured, and myeloperoxidase activity in colon tissue was also examined. Histological lesions, morphological damage, and myeloperoxidase activity were reduced after 1 week of treatment with berberine at a dosage of 15 mg/kg/day. Furthermore, 1 week after trinitrobenzene sulfonic acid treatment, the production of interleukin-8 by cultured rectal mucosa or cardiac blood mononuclear cells with or without stimulation of lipopolysaccharide for 24 h was also analyzed by enzyme-linked immunosorbent assay. Cardiac blood mononuclear cells and rectal mucosa of normal rats produced substantial amounts of interleukin-8, which increased strikingly with the stimulation of lipopolysaccharide. Cardiac blood mononuclear cells and rectal mucosa of trinitrobenzene sulfonic acid-treated rats secreted more interleukin-8 than those of normal rats. The addition of berberine with a concentration of 10(-5) M to the culture media resulted in an inhibition of interleukin-8 production of rectal mucosa.
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PMID:The effect of berberine chloride on experimental colitis in rats in vivo and in vitro. 1094 29

We previously reported that intracolonic administration of enprostil, a prostaglandin-E(2) (PGE(2)) analogue, had therapeutic effects on acute colitis induced in rodents by dextran sulfate sodium (DSS). In addition, production of growth-regulated gene product/cytokine-induced neutrophil chemoattractant-1 [GRO/CINC-1; an interleukin(IL)-8 like cytokine] was suppressed in the inflamed tissues. In the present study we used a human colon cancer cell line (HT-29) to investigate enprostil effects on the IL-8 production of intestinal epithelial cells stimulated by various stimulants. In a MTT assay, concentrations of enprostil >10(-5)M had cytotoxitic effects on HT-29 cells. Furthermore, 10(-6) M enprostil suppressed IL-8 production in HT-29 cells, SW620 and CaCo2 stimulated with interleukin-1 beta (IL-1 beta) or lipopolysaccharide (LPS), but did not suppress this response when cells were stimulated with tumour necrosis factor (TNF)-alpha. These results suggest that enprostil affects a point in the pathway between the IL-1 receptor or LPS receptor and nuclear factor-kappa B(NF-kappa B), without affecting the pathway between the TNF receptor and NF-kappa B, with the latter factor being required for the IL-8 gene transcription. The therapeutic effect of exogenous enprostil on DSS colitis may involve the inhibition of IL-8 production in colonic epithelial cells stimulated by IL-1 beta or LPS.
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PMID:Enprostil, a prostaglandin-E(2) analogue, inhibits interleukin-8 production of human colonic epithelial cell lines. 1111 62

The influence of biallelic polymorphisms in the tumour necrosis factor-alpha (TNF alpha), lymphotoxin-alpha (LT alpha) and interleukin-10 (IL-10) genes on stimulated TNF alpha and IL-10 production was studied in ulcerative colitis (UC) patients, Crohn's disease (CD) patients and in healthy controls. A polymerase chain reaction sequence-specific primer (PCR-SSP) system was developed to type nine biallelic polymorphisms, three in each of the TNF alpha, LT alpha and IL-10 genes. Production of the TNF alpha and IL-10 was measured by ELISA in lipopolysaccharide (LPS) stimulated whole blood. Four haplotypes of the TNF alpha gene, three haplotypes of LT alpha and three haplotypes of IL-10 were identified. No significant differences in haplotype frequencies were found between patients and controls overall. On subgroup analysis however, haplotype TNF-2 was more frequent in women with extensive colitis compared to distal colitis (31% vs 12%; P = 0.028). This difference was even greater for the combined TNF-2-LT alpha-2 haplotype (56% vs 21%; P = 0.0007). The TNF-2 and LT alpha-2 haplotypes were associated with higher TNF alpha production in CD patients, and the TNF-4 haplotype was associated with lower TNF alpha production in UC patients. The A allele in the IL-10 promoter region at position -1082 was associated with decreased IL-10 production in CD patients and controls (P = 0.005, P = 0.015 respectively). These data provide evidence that the effect of TNF alpha, LT alpha and IL-10 gene polymorphisms on cytokine production differ in CD, UC patients and controls.
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PMID:Cytokine (TNF alpha, LT alpha and IL-10) polymorphisms in inflammatory bowel diseases and normal controls: differential effects on production and allele frequencies. 1119 10


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