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)

Alterations in peripheral blood neutrophil function are known to occur in patients with colitis and may have a role in precipitating nonspecific tissue injury. It is not known whether neutrophil function is altered in patients with Shigella dysenteriae type 1 infection, during which there is extensive colitis and which may be associated with life-threatening complications in young children. Three aspects of peripheral blood neutrophil function, polarization, attachment to yeast particles, and locomotion, were therefore studied in 111 children with S. dysenteriae type 1 infection and 57 children without any infection. All children were aged 12 to 60 months. Of the children with S. dysenteriae type 1 infection, 42 had leukemoid reaction, hemolytic-uremic syndrome, or septicemia (complicated shigellosis), while the others did not (uncomplicated shigellosis). Polarization and locomotion in the absence of chemoattractants and in response to N-formylmethionyl-leucylphenylalanine (FMLP) and the lipopolysaccharide (LPS) of S. dysenteriae type 1 were determined. Attachment to unopsonized and opsonized yeast particles was also determined. Children with shigellosis (uncomplicated or complicated) had more polarized neutrophils with and without chemoattractants than uninfected children (P < 0.05). Children with complicated shigellosis had more polarized neutrophils with FMLP at 10(-7) and 10(-6) M (P < 0.05) and with LPS than children with uncomplicated shigellosis (P < 0.05). At 3 to 5 days after enrollment, the numbers of polarized neutrophils with 10(-8), 10(-6), and 10(-5) M FMLP declined in children with uncomplicated shigellosis but not in those with complicated shigellosis. Attachment to yeast particles was similar in all three groups of children. Locomotion was inhibited by LPS in children with shigellosis (P < 0.05), whether it was uncomplicated or complicated, compared with locomotion in uninfected children. Finally, neutrophil polarization in uninfected children was negatively influenced by nutritional status. Thus, poorly nourished uninfected children had more polarized neutrophils with FMLP at 10(-9) M (P < = 0.02) and 10(-5) M (P = 0.043) than their better-nourished counterparts. In summary, altered neutrophil responses are associated with both uncomplicated and complicated shigellosis.
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PMID:Peripheral blood neutrophil responses in children with shigellosis. 854 43

The acute phase of inflammation induces both anorexia and fever. Because several analyses suggest a linkage between the meal size and body temperature, we assessed whether temperature changes were causal to anorexia in situations involving acute inflammation. Specifically, we evaluated whether elevations of body temperature could account for the reduced food intake after induction of experimental colitis [via intrarectal infusions of trinitrobenzene sulfonic acid (TNB)] or injection of 100 micrograms/kg lipopolysaccharide (LPS). Temperature was monitored telemetrically in rats via implanted temperature transmitters. TNB-treated rats demonstrated a 5-day anorexia that resulted specifically from a decrease in meal size. Although TNB-treated rats were hypothermic on the day of treatment, no other body temperature changes were noted. LPS reduced food intake and elevated temperature, but these two effects were uncorrelated temporally. Although these results do not identify the mechanisms of anorexia, the findings indicate clearly that the anorexia associated with the acute inflammatory response is not secondary to fever.
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PMID:Dissociation of temperature changes and anorexia after experimental colitis and LPS administration in rats. 889 89

The effects of the Lps gene on the development of experimental ulcerative colitis were studied in two genetically different mouse strains: C57B1 and C3H. Acute colitis was induced by adding 3% dextran sulfate sodium (DSS) to the drinking water for a 7-day (C57B1 and C3H) or a 10-day (C57B1) experimental period. Although the DSS treatment initiated the same type of morphological changes in the colon in all groups of mice, an earlier onset and persistent intestinal bleeding occurred in the Lpsn mice (sensitive to lipopolysaccharide, LPS) in comparison with the Lpsd mice (hyporesponsive to LPS). Rectal bleeding appeared on day 7 in 90% of the Lpsn compared to 13% of the Lpsd mice (p < 0.0001). In C57B1 mice, followed for three additional days, 50% of the Lpsn mice died and the surviving animals showed as well as rectal bleeding a large number of Gram-negative bacteria in the liver and spleen. In contrast, the Lpsd mice of the C57B1 strain appeared unaffected by the treatment, although a transient rectal bleeding occurred in 90% on day 8. Also, significantly fewer Gram-negative bacteria were found in the liver and spleen. Even though significantly increased serum endotoxin levels were seen in all DSS-treated groups compared to controls on day 7, the serum levels of TNF alpha were significantly increased only in the Lpsn mice. In DSS-induced colitis the Lpsn genotype conferred on the mice an increased LPS susceptibility, resulting in an augmentation of the inflammatory response to Gram-negative bacteria and their endotoxins. The results suggest that LPS-induced host effector mechanisms significantly enhanced the intestinal bleeding, systemic inflammatory response, and mortality in mice with DSS-induced colitis. In addition, the host defense against the invading and systemically spread bacteria most probably involved additional genes.
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PMID:The role of the Lps gene in experimental ulcerative colitis in mice. 898 46

Identification of the O157 antigen is an essential part of the detection of Escherichia coli O157:H7, which is recognized as a major etiologic agent of hemorrhagic colitis. However, polyclonal antibodies produced against E. coli O157:H7 lipopolysaccharide (LPS) may react with several other bacteria including Brucella abortus, Brucella melitensis, Yersinia enterocolitica O9, Escherichia hermannii, and Stenotrophomonas maltophilia. We produced eight monoclonal antibodies (MAbs) specific for the LPS of E. coli O157. Western blots (immunoblots) of both the phenol phase (smooth) and the aqueous phase (rough) of hot phenol-water-purified LPS indicated that three of the MAbs were specific for the O antigen and five were reactive with the LPS core. The eight MAbs could be further differentiated by their reactivities to Salmonella O30 LPS (group N), which is reported to be identical to the E. coli O157 antigen. All eight MAbs reacted strongly to all of the 64 strains of E. coli O157 tested, which included 47 isolates of O157:H7 and 17 other O157 strains. None of the eight MAbs cross-reacted with any of the 38 other E. coli serotypes tested, which consisted of 29 different O-antigen serotypes, or with 38 strains (22 genera) of non-E. coli gram-negative enteric bacteria.
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PMID:Production and characterization of monoclonal antibodies specific for the lipopolysaccharide of Escherichia coli O157. 904 12

In 1994-1996 summer, eight patients with hemolytic uremic syndrome(HUS) and 3 patients with hemorrhagic colitis, whose fecal specimens yielded no Enterohemorrhagic Escherichia coli(EHEC) because of the antibiotic therapies before presentation, showed serum IgM antibody responses to lipopolysaccharide(LPS) of O157. Although early bacteriological examination is essential for diagnosis, serological testing of patients with HUS or HC for antibodies to the LPS of EHEC provides evidence of infection with EHEC. We also presented successful fluoroquinolones(SPFX and NFLX) therapies of another 15 HC inpatient cases from Sakai outbreak of O157 infections due to school lunch in summer 1996. In these 15 HC patients, 12 EHECs of serotype O157:H7 with VT1 and VT2 and phage type 32 were obtained, but no growths of EHECs after fluoroquinolones therapy and no progressions to HUS resulted. The MICs of SPFX is 0.025 microgram/dl, NFLX 0.1, NA 3.13, FOM 12.5, ST 0.39, KM 3.13, ABPC 1.56-3.13.
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PMID:[Sporadic cases of hemolytic uremic syndrome and hemorrhagic colitis with serum IgM antibodies to lipopolysaccharides of enterohemorrhagic Escherichia coli O157]. 908 82

Serum immunoglobulin (Ig) titres to core lipopolysaccharide (LPS) were determined in 102 horses admitted to a university referral hospital during a 12-month period for evaluation of colic. Serum samples were collected again 10-14 days later from 84 of the horses. Titres to core LPS were quantitated by an indirect enzyme-linked immunosorbent assay (ELISA), utilising the J-5 mutant of Escherichia coli 0111:B4 as the solid-phase antigen. All horses had natural antibodies to core LPS at the time of admission and the titre was not affected significantly by age, sex or type of gastrointestinal disorder. The geometric mean titres to core LPS increased significantly within 14 days of admission in those horses with large colon displacement (25), ileal impaction (13), small intestinal strangulating obstruction (11) and small colon obstruction (4). Twenty four (28.6 per cent) of the horses had at least a 4-fold rise in titre (seroconversion) to core LPS within 14 days of admission. The incidence of seroconversion to core LPS was significantly greater (P < 0.05) in horses with disorders requiring surgical intervention (35.8 per cent) than in those with disorders (proximal enteritis, colitis, large colon impaction and unknown) which only required medical treatment (16.1 per cent). Seroconversion rate was not statistically different between groups of horses with diseases of the small intestine which required surgical or medical treatments. The results of this study indicate that gastrointestinal disorders that cause colic in horses result in IgG production to core LPS, and the latter is more prevalent in disorders requiring surgery.
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PMID:Antibody titres to core lipopolysaccharides in horses with gastrointestinal disorders which cause colic. 911 2

We have observed a rapid induction of manganese superoxide dismutase (MnSOD) in epithelial, neuronal, and smooth muscle cells (SMC) after acetic acid-induced colitis. To examine the regulation of MnSOD in the SMC more specifically, primary cultures of colonic SMC were developed by enzymatic digestion of the circular muscle layer from an adult rat. SMC were treated for 2-72 h with 0.5 microgram/ml Escherichia coli endotoxin [lipopolysaccharide (LPS)], 10 ng/ml tumor necrosis factor (TNF)-alpha, or 2 ng/ml interleukin-1 beta (IL-1 beta). Cotreatments were performed with IL-1 beta and 4 microM actinomycin or 50 microM cycloheximide. Northern analysis demonstrated 23-fold, 8-fold, and 6-fold inductions of MnSOD mRNA by IL-1 beta, LPS, and TNF-alpha, respectively. Induction of MnSOD by IL-1 beta was eliminated by actinomycin but not by cycloheximide, implicating a requirement for de novo transcription. Western analysis resulted in a 23.7-fold induction of MnSOD protein after 48-h treatment with IL-1 beta. Induction of MnSOD by IL-1 beta and other inflammatory mediators may serve as a protective mechanism to reduce oxygen free radical- and nitric oxide-mediated cell damage during inflammation.
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PMID:Regulation of superoxide dismutase in primary cultures of rat colonic smooth muscle cells. 917 34

Interleukin-11 (IL-11) is a stromal cell-derived cytokine with several biological activities against hematopoietic cells. Recent results indicated that IL-11 reduced mucosal damage in animal models of colitis. This study aimed to explore the action of recombinant human IL-11 (rhIL-11) on the intestinal effects of Clostridium difficile toxin A, an inflammatory enterotoxin, and cholera toxin, a noninflammatory enterotoxin in rat ileum. We administered rhIL-11 subcutaneously to rats before injection of toxin A into ileal loops and measured fluid secretion, epithelial permeability to mannitol, histopathological damage, and release of rat mast cell protease II (RMCP II) from intestinal mast cells and of tumor necrosis factor-alpha (TNF-alpha) and macrophage inflammatory protein-2 (MIP-2) from lamina propria macrophages. rhIL-11 (50-1,000 micrograms/kg) inhibited toxin A but not cholera toxin-mediated secretion and permeability in a dose-dependent fashion and reduced toxin A-induced epithelial cell damage. Rats treated with rhIL-11 also showed reduced RMCP II, TNF-alpha, and MIP-2 release in response to toxin A. Exposure of rat peripheral monocytes in vitro to rhIL-11 (1 microgram/ml) inhibited lipopolysaccharide and toxin A-mediated increases in TNF-alpha mRNA and protein levels. We conclude that rhIL-11 blocks the intestinal effects of C. difficile toxin A, possibly by inhibiting release of inflammatory mediators from mucosal mast cells and intestinal macrophages.
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PMID:IL-11 inhibits Clostridium difficile toxin A enterotoxicity in rat ileum. 927 11

An outbreak of food poisoning due to Escherichia coli O157 phage type 2 Vero cytotoxin 2 affected 26 people in southern counties of England in May and June 1995. The organism was isolated from faecal specimens from 23 patients, 16 of whom lived in Dorset and seven in Hampshire. Isolates were indistinguishable by phage typing, Vero cytotoxin gene typing, restriction fragment length polymorphism, and pulsed field gel electrophoresis. Three associated cases, linked epidemiologically to the outbreak, were confirmed serologically by detection of antibodies to E. coli O157 lipopolysaccharide. Twenty-two of the 26 patients were adults: four were admitted to hospital with haemorrhagic colitis. Four cases were children: two were admitted to hospital with haemolytic uraemic syndrome (HUS). There were no deaths. Although E. coli O157 was not isolated from any food samples, illness was associated with having eaten cold meats in sandwiches bought from two sandwich producers, in Weymouth and in Portsmouth. Both shops were supplied by the same wholesaler, who kept no records and obtained cooked meats from several sources in packs that did not carry adequate identification marks. It was, therefore, impossible to trace back to the original producer or to investigate further to determine the origin of contamination with E. coli O157. To protect the public health it is essential that all wholesale packs of ready-to-eat food carry date codes and the producer's identification mark. Detailed record keeping should be part of hazard analysis critical control point (HACCP) systems and should be maintained throughout the chain of distribution from the producer to retail outlets.
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PMID:An outbreak of Vero cytotoxin producing Escherichia coli O157 infection associated with takeaway sandwiches. 944 85

Shiga toxin-producing Escherichia coli (STEC) are a diverse group of organisms known to cause diarrhoea, haemorrhagic colitis and haemolytic uraemic syndrome (HUS) in humans. During the early stage of infection, numbers of STEC in the gut may be very high (of the order of 10(9)/g faeces), but as disease progresses, the numbers may drop rapidly such that STEC are undetectable within a week. Convalescent sera from patients recovering from HUS frequently contain high levels of antibody to E. coli lipopolysaccharide (LPS) of the infecting serotype, and it is possible that a local immune response to LPS contributes to elimination of the organism from the gut. We have recently demonstrated that STEC strains isolated from HUS cases have enhanced adherence to a human intestinal epithelial cell line (Henle 407) compared with STEC strains from non-human sources. In this study, we examined the capacity of STEC strains belonging to O-antigen types O111 and O157 to adhere to human intestinal epithelial (Henle 407) cells in the presence or absence of anti-LPS. Adherence was inhibited by up to 95% by anti-LPS of the homologous, but not heterologous serotype. This effect was not an artefact of serum bactericidal or agglutinating activity. Preincubation with purified homologous or heterologous LPS did not prevent adherence, suggesting that LPS was not acting as an adhesin per se. Nevertheless, these findings raise the possibility that oral administration of preparations containing anti-LPS may interfere with colonization of the human gut by STEC, and therefore could be of potential therapeutic value if administered early in the course of infection.
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PMID:Antibodies to lipopolysaccharide block adherence of Shiga toxin-producing Escherichia coli to human intestinal epithelial (Henle 407) cells. 946 47


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