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)

In this study, 27 volunteers received one of three non-O group 1 Vibrio cholerae strains in doses as high as 10(9) CFU. Only one strain (strain C) caused diarrhea: this strain was able to colonize the gastrointestinal tract, and produced a heat-stable enterotoxin (NAG-ST). Diarrhea was not seen with a strain (strain A) that colonized the intestine but did not produce NAG-ST, nor with a strain (strain B) that produced NAG-ST but did not colonize. Persons receiving strain C had diarrhea and abdominal cramps. Diarrheal stool volumes ranged from 154 to 5,397 ml; stool samples from the patient having 5,397 ml of diarrhea were tested and found to contain NAG-ST. The median incubation period for illness was 10 h. There was a suggestion that occurrence of diarrhea was dependent on inoculum size. Immune responses to homologous outer membrane proteins, lipopolysaccharide, and whole-cell lysates were demonstrable with all three strains. Our data demonstrate that V. cholerae of O groups other than 1 are able to cause severe diarrheal disease. However, not all strains are pathogenic for humans: virulence of strain C may be dependent on its ability both to colonize the intestine and to produce a toxin such as NAG-ST.
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PMID:Experimental non-O group 1 Vibrio cholerae gastroenteritis in humans. 231 21

We genetically modified attenuated Salmonella typhi strain Ty21a to express the form I O polysaccharide antigen of Shigella sonnei. Three doses of this bivalent, live oral vaccine strain (1-8 X 10(9) organisms/dose) were given to young adults who, along with unvaccinated controls, were challenged one month later with pathogenic S. sonnei. The vaccinees had 40% protection against diarrhea and 56% against Hematest-positive diarrhea. Two of three vaccine lots provided higher levels of protection (53% against diarrhea and 71% against Hematest-positive diarrhea), but the third lot, prepared for a large-scale field trial, demonstrated no protective efficacy. Vaccinees had serum and local intestinal immune responses to S. sonnei lipopolysaccharide, and the presence of specific serum IgA or IgG antibody before challenge with pathogenic S. sonnei was correlated with protection from illness. Some lots of this bivalent vaccine strain provide significant protection against S. sonnei disease, but the problem of lot-to-lot variability must be overcome.
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PMID:Prevention of shigellosis by a Salmonella typhi-Shigella sonnei bivalent vaccine. 243 20

Mice immunised by the oral or intraperitoneal route with a live aromatic-dependent strain of Salmonella typhimurium exhibited significantly less protection against oral challenge with 50 LD50 of an ovine isolate of S. typhimurium (12313) than when a bovine isolate with the same O antigens and phage-type as strain 12313 was used as the challenge organism. When challenged with 10 LD50, however, protection against both strains was significantly better than that obtained when mice were vaccinated with killed vaccines (heat-killed, acetone-killed or irradiated) even when the antigenic mass of the killed vaccine was increased by up to 500-fold in an attempt to compensate for the expected limited multiplication of the mutant organism. Sheep immunised with the live mutant strain by either the intramuscular or oral route were protected against oral challenge with the virulent ovine isolate of S. typhimurium; unimmunised sheep died of acute enteritis within 7 days, although there was no evidence of systemic invasion by the challenge organism. After challenge, immunised animals ate more food than the unimmunised controls and suffered only transient, mild diarrhoea. Serum antibody titres against O and H antigens measured by direct or antiglobulin tests were significantly higher in sheep immunised by the intramuscular route than in those immunised orally. Sheep in both immunised groups developed skin swellings within 30 min after intradermal inoculation with purified homologous lipopolysaccharide indicating development of immediate-type hypersensitivity, but only those immunised by the intramuscular route showed significant indurated skin swellings characteristic of delayed-type hypersensitivity 48 and 72 h post-inoculation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Protection against experimental salmonellosis in mice and sheep by immunisation with aromatic-dependent Salmonella typhimurium. 244 Oct 60

Water extracts of Escherichia coli "O" and "K" antigen test strains (EPEC, ETEC, EIEC, UPEC) were examined in immunodiffusion and immunoelectrophoresis tests. The precipitation arcs corresponding to the O-antigen specificity and to the thermostable polysaccharide K antigen were easy to identify. All strains gave an O antigen precipitation arc found either on the anodic or the cathodic side of application basin and close to this. The so-called enteropathogenic types (from infantile diarrhoea) had a cathodic O antigen arc type; from dysentery-like disease had a negatively charged O-antigen, but no special thermostable K-antigen. Thus E. coli strains which may invade the tissues when conditions allow have a negatively charged surface antigen, either O-antigen lipopolysaccharide or both. Acidic components were found in the anodic O-antigen.
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PMID:[Immunoelectrophoretic analysis of Escherichia coli strains (EPEC, ETEC, EIV and UPEC) (1)]. 244 16

Adhesion of Campylobacter jejuni and C. coli to epithelial cells is thought to be a decisive step in enteritis. In this work, we tried to determine which bacterial components are responsible for this phenomenon. Outer membrane (OM) extracts were prepared from strains of C. jejuni (3 strains) and C. coli (2 strains). These strains had been isolated from stools of febrile patients with diarrhoea and were able to adhere to HeLa cells in culture. After incubation of bacterial OM extracts with HeLa cells in culture, bacterial adherent material was recovered, subjected to electrophoresis and immunoblotted. Bacterial adherent antigens were revealed by a rabbit antiserum raised against whole bacterial cells. Antigenic fractions, ranging from 26 to 30 kDa, were found to preferentially bind to HeLa cells (cell-binding fractions; CBF). These antigens were proteins and were distinct from flagellin and lipopolysaccharide. Bacteria incubated with a rabbit antiserum raised against homologous CBF, were unable to bind to HeLa cells. Moreover, the inhibitory effect decreased when the antiserum was diluted. Under the same conditions, a rabbit antiserum raised against a non-adherent OM fraction of 92 kDa did not prevent bacteria from binding to HeLa cells.
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PMID:Adhesion to HeLa cells of Campylobacter jejuni and C. coli outer membrane components. 261 91

Endotoxins (lipopolysaccharides, LPS) are potent bacterial poisons always present within the intestines in considerable amounts. Several pathophysiological conditions such as hypovolaemia, hypoxia, intestinal ischaemia, burns and radiation lead to a breakdown in the barrier and depending upon the extent of the injury, endotoxins enter the systemic circulation in increasing amounts. Antibiotics do not inactivate the endotoxins which continue to exert their toxic effects leading to nausea, vomiting, diarrhoea, fever, disseminated intravascular coagulation, vascular collapse and organ failure. When nonabsorbable antibiotics are given prior to the insult, systemic endotoxaemia is prevented. Immunotherapy, using anti-lipopolysaccharide IgG, inactivates plasma endotoxins, destroys gram-negative bacteria and opsonises them and may become a major form of therapy. An outline of endotoxin and anti-lipopolysaccharide and its importance to the anaesthetist and intensive care specialist is presented.
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PMID:Endotoxins and anti-endotoxins (their relevance to the anaesthetist and the intensive care specialist). 265 93

An adult Bangladeshi woman had persistent bloody diarrhea. Repeated stool cultures yielded Plesiomonas shigelloides in pure growth. Tissue specimens of the colon were consistent with pseudomembranous colitis. Treatment with tetracycline, to which the isolate was susceptible, brought prompt recovery; the stool cultures became negative and the serum antibody titer against P. shigelloides lipopolysaccharide, as measured by hemagglutination inhibition with P. shigelloides lipopolysaccharide-sensitized sheep erythrocytes, declined from 1:160 to 1:40.
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PMID:Case report of Plesiomonas shigelloides-associated persistent dysentery and pseudomembranous colitis. 276 77

Escherichia coli that exhibit the aggregative pattern of adherence to HEp-2 cells (enteroadherent-aggregative E. coli [EA-AggEC]) have been epidemiologically incriminated as a cause of diarrhea. We undertook a preliminary microbiological and pathogenetic characterization of 42 isolates of this putative pathogen. The strains were negative by tests with DNA probes for enteropathogenic, enterotoxigenic, enteroinvasive, and enterohemorrhagic E. coli and, by serotype, did not fit these categories. Thirty-nine of 42 strains had a 55-65-megadalton plasmid; many shared DNA homology. With one representative strain, plasmid transfer was accompanied by transfer of smooth lipopolysaccharide, fimbriae expression, and the aggregative property. EA-AggEC caused characteristic lesions in rabbit and rat ileal loops. The intestinal lesions and (Shiga-like) limb paralysis and death in rabbits inoculated with live organisms suggest toxin involvement; assays for Shiga-like toxins were negative. These preliminary results support the contention that EA-AggEC may represent a distinct category of diarrheagenic E. coli.
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PMID:Characterization of enteroadherent-aggregative Escherichia coli, a putative agent of diarrheal disease. 289 25

Subcutaneous challenge of mice with lipopolysaccharide (LPS) from gram negative bacteria, produced an intestinal microvascular lesion causing fluid exudation into the lumen of the intestine and diarrhea. The microvascular lesion was characterized by endothelial cell damage and microthrombi in the venules and capillaries of the intestinal lamina propria. Marker organisms, given orally to challenged mice, grew in the exuded fluid and could invade the mucosa. Intravenous transfer of postchallenge plasma produced the lesion in normal mice and absorption of such plasma by Sepharose coupled to LPS-antibody abolished this effect. Instillation of large quantities of LPS into the lumen of the intestine produced scattered microvascular lesions, although none of these animals developed diarrhea. Since a similar microvascular lesion has been described in the rectal mucosal lamina propria of adults with acute diarrhea, it is suggested that LPS-induced vascular damage may be a novel mechanism in the pathogenesis of acute diarrhea.
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PMID:Bacterial lipopolysaccharide-induced intestinal microvascular lesions leading to acute diarrhea. 318 65

Cholera disease can be induced in the rabbit by ligation of the cecum (C) followed by duodenal inoculation (DI) of virulent Vibrio cholerae organisms (DIC model). When the cecum is not ligated, DI does not induce disease. In contrast, the animals are primed which becomes apparent upon challenge with live V. cholerae in the DIC model. Such animals are vibriocidally protected. This protection is characterized by absence of disease symptoms, rapid disappearance of V. cholerae from the feces and presence of high levels of anti-lipopolysaccharide Immunoglobulin A in the bile. The present study shows that primed rabbits can also be boosted by duodenal administration of killed, smooth V. cholerae cells. On the other hand, killed cells cannot prime. The minimal lethal dose of a rough derivative of a smooth strain C5, designated R5 and lacking the O antigen part of the LPS, was 100,000 times higher than that of its parent strain C5, in the DIC model. Rabbits which had been duodenally immunized with strain R5 and were subsequently challenged with the smooth strain C5, all developed diarrhea and two out of eight died. This result supports an earlier observation that the specific O antigen part of the V. cholerae LPS is an essential prerequisite for the induction of protective immunity in the rabbit.
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PMID:Priming and boosting of the rabbit intestinal immune system with live and killed, smooth and rough Vibrio cholerae cells. 320 Jan 61


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