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Query: UNIPROT:P43026 (lipopolysaccharide)
 62,215 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To study the secretory immune response after Shigella infection, the anti-lipopolysaccharide and anti-Shiga-toxin response in saliva, obtained from children with confirmed shigellosis and healthy children, were determined by enzyme-linked immunosorbent assay and by Western blot. Children with infection showed high titers compared to healthy controls. After Shigella dysenteriae type 1 infection a significant change in titer could be observed in a large number of cases, in contrast to Shigella flexneri infection. It appeared that, in children living in endemic areas, infection with one serotype can give a rise in antibody titer to another serotype. This could be ascribed to polyclonal B cell activation since children in endemic areas routinely show relatively high titers to Shigella antigens. We conclude that the dynamics of salivary anti-Shigella LPS and anti-Shiga-toxin in children with dysentery indicate that it can be applied to studies of immune response in shigellosis for epidemiological and vaccination purposes.
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PMID:Shigella-specific IgA in saliva of children with bacillary dysentery. 154 24

This study explores the in vitro relationship between Shiga toxin-producing Shigella spp. and Escherichia coli and the development of vascular complications in humans following bacillary dysentery. We propose that lipopolysaccharide (LPS; endotoxin) may combine with Shiga toxin to facilitate vascular damage characteristic of hemolytic uremic syndrome. We have examined the direct cytotoxic effects of Shiga toxin and LPS on human umbilical vein endothelial cells (HUVEC) in culture. Shiga toxin alone was cytotoxic to HUVEC, whereas LPS was noncytotoxic at concentrations at or below 10 micrograms/ml. Combinations of LPS with Shiga toxin resulted in a synergistic cytotoxic effect. The synergistic cytotoxic response of HUVEC to Shiga toxin plus LPS was dose dependent for both agents and was maximal at 24 h of exposure. This synergistic response was enhanced by preincubation of HUVEC with LPS. LPS (1 micrograms/ml) alone depressed HUVEC protein synthesis in a transient manner and enhanced the protein synthesis-inhibiting activity of Shiga toxin. The synergistic cytotoxic activity of LPS analogs was as follows, in decreasing order: complete LPS = diphosphoryl lipid A greater than monophosphoryl lipid A greater than deacylated LPS. These results are consistent with a role for Shiga toxin and LPS in the development of hemolytic uremic syndrome at the level of the vascular endothelium in humans.
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PMID:Shiga toxin-associated hemolytic uremic syndrome: combined cytotoxic effects of shiga toxin and lipopolysaccharide (endotoxin) on human vascular endothelial cells in vitro. 154 77

An indirect hemagglutination assay consisting of sheep erythrocytes coated with lipopolysaccharide (LPS) from Shiga-like toxin-producing Escherichia coli O157 was used for the serological diagnosis of E. coli O157 infections in children with classical (enteropathic) hemolytic-uremic syndrome (HUS). One week after the onset of diarrhea (acute phase of the disease), the E. coli O157 antibody titer was greater than or equal to 1:4,096 in 22 of 27 patients with HUS, compared with 4 of 249 controls, the majority of whom had O157 antibody titers of between 1:4 and 1:256. This antibody response was observed in HUS patients with stool cultures positive and negative for E. coli O157. Selective absorption with homologous LPS and heterologous LPS showed that the antibody response was specific for E. coli O157. Because of its simplicity and ease of interpretation, the indirect hemagglutination assay described in this paper is recommended for the serological diagnosis of E. coli O157 infections in patients with HUS.
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PMID:Indirect hemagglutination assay for diagnosis of Escherichia coli O157 infection in patients with hemolytic-uremic syndrome. 158 16

Only indirect evidence has been cited to document that lipopolysaccharide-mediated virulence at the bacterial level and serum antibodies to the O-specific side chain of the lipopolysaccharide molecule may prevent shigellosis. Our proposed use of the B subunit of Shiga toxin as a carrier protein is based upon evidence (even more indirect) that serum antitoxin may reduce the severity of dysentery and diarrhea. Because animal models of disease may provide information inapplicable to the prediction of vaccine-induced protective immunity, we suggest that clinical trials in the population at risk should be started after successful completion of the safety and immunogenicity phases of vaccine development in laboratory animals and in the target population. Clinical studies of shigella vaccines are difficult because of the many causes of dysentery in a population with a high rate of intestinal disease.
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PMID:O-specific side-chain toxin-protein conjugates as parenteral vaccines for the prevention of shigellosis and related diseases. 204 64

Seven strains of inbred mice were compared for their susceptibility to the lethal effects of Shiga-like toxin II (SLT II). A/J mice, which are unable to produce the C5 component of complement, did not differ from C5 normal mice in susceptibility to SLT II. CBA/NJ mice (hemizygous for X-linked immunodeficiency) did not differ from the B-cell sufficient CBA/J strain. C3H/HeJ mice, defective in macrophage response to lipopolysaccharide (Lpsd), showed a consistently and significantly longer mean time to death than did the normally responsive C3H/HeN strain. C57BL/10ScN mice, which also carry the Lpsd allele, showed a similar but smaller difference in mean time to death compared with the C57BL/10SnJ strain. Production of tumor necrosis factor could be induced in vitro by SLT II treatment of C3H/HeN, but not C3H/HeJ macrophages. These results imply that antibody and complement production do not modulate SLT II lethality in mice, but that the macrophage may contribute to SLT II-induced injury.
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PMID:Evidence for participation of the macrophage in Shiga-like toxin II-induced lethality in mice. 227 89

According to the literature and the authors' data in patients who died of dysentery Shigellae are found seldom because of postmortem shedding of superficial colonic epithelium infected by them. Shigella adhesion and invasion into the colonocytes are regularly found in the colon biopsies. As shown recently in experiments, Shigella outer membrane proteins forming "contact haemolysin" ("virulence plasmid" product) are responsible for their invasion. In the small intestine this cytotoxin is destroyed by trypsin, therefore Shigella invasion takes place in the large intestine where it also lyses vacuole membranes around the bacteria in colonocytes. Widespread cytopathic alterations of the epithelium with a damage to ribosome and protein synthesis, disturbance of vascular permeability and fluid hypersecretion in the small intestine result from Shiga-like enterotoxin-cytotoxin. Extent of the inflammatory leukocyte response depends on the degree of Shigella invasion and multiplication and the destruction of the epithelium. Damages to the endothelium and blood coagulation system resulting occasionally in the infectious-toxic shock, are associated with Shigella destruction by leukocytes and absorption of lipopolysaccharide endotoxin released by them. Interepithelial lymphocytes especially those containing lysosome-like granules (similar to the blood "natural killers") play an important role in the response to Shigella.
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PMID:[Current views on the pathomorphology and pathogenesis of dysentery]. 228 80

Recent studies have shown that determinants for the production of O antigen lipopolysaccharide in Shigella dysenteriae 1 are distributed over two distinct genetic elements, the chromosome and a 9 kb plasmid designated pHW400. In this communication, we describe the cloning of all determinants necessary for S. dysenteriae 1 O antigen production in E. coli K-12 and their combination in a single plasmid. An RP4::miniMu R-prime plasmid, R-prime 40, containing the his-rfb (histidine biosynthesis-lipopolysaccharide biosynthesis) gene region of the Shigella dysenteriae 1 chromosome was generated. E. coli K-12 bacteria containing R-prime 40 and pSS8, a transposon Tn5-tagged derivative of pHW400, produced lipopolysaccharide indistinguishable from that of S. dysenteriae 1. Small DNA fragments containing the rfb gene cluster and the rfp gene were subcloned from R-prime 40 and pSS8 and subsequently combined in vector pACYC184 to produce pSS37. This latter plasmid when introduced by transformation into E. coli K-12 provoked the formation of S. dysenteriae 1 O-specific lipopolysaccharide, a feature that suggests it may be useful in the construction of LPS-based live vaccines against the Shiga bacillus.
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PMID:Cloning of the rfb gene region of Shigella dysenteriae 1 and construction of an rfb-rfp gene cassette for the development of lipopolysaccharide-based live anti-dysentery vaccines. 246 31

The ability of bacterial lipopolysaccharide (LPS) to enhance the toxicity of Shiga-like toxin II (SLT-II) was investigated in rabbits and mice. Rabbits were continuously infused with 0.5 50% lethal dose (LD50) of SLT-II per day. Rabbits that received a 30-micrograms/kg dose of LPS (0.02 LD50) on day 3 of infusion were significantly more likely to die than were rabbits receiving SLT-II only. Rabbits receiving SLT-II and a lower dose of LPS (3 micrograms/kg) did not die but lost an average 3.3% +/- 1.0% of initial body weight during the first 5 days of infusion, compared with weight gains of 4.2% +/- 0.6% and 17.1% +/- 0.9% for rabbits receiving only SLT-II or LPS, respectively. Rabbits that were pretreated with LPS 20 h before challenge with a single dose of SLT-II showed highly significant protection from both the diarrheagenic and lethal effects of SLT-II. Pretreatment of endotoxin-responsive C3H/HeN mice protected the animals from challenge with an LD50 but not an LD100 of SLT-II. LPS enhanced the lethal toxicity of SLT-II for C3H/HeN mice when it was given at 8 or 24 h but not 0 or 72 h after SLT-II challenge. LPS did not affect the lethal toxicity of SLT-II for endotoxin-resistant C3H/HeJ mice. These results suggest that LPS enhances the effects of SLT-II in vivo. Since cecal changes that increase mucosal permeability occur in response to SLT in rabbits, this synergy may be directly relevant to disease processes.
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PMID:Bacterial endotoxin both enhances and inhibits the toxicity of Shiga-like toxin II in rabbits and mice. 268 Sep 74

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

The requirement for both plasmid and chromosomal genes in the biosynthesis of Shigella dysenteriae 1 lipopolysaccharide O antigen was demonstrated in Escherichia coli-Shigella hybrids. A 6-megadalton S. dysenteriae 1 plasmid, designated pWR23, was phenotypically tagged with the Tn3 ampicillin-resistance transposon. The tagged plasmid, designated pWR24, was transferred by transformation or conjugal mobilization to a rough E. coli K-12 recipient. Although the resultant hybrids were agglutinated in S. dysenteriae 1 antiserum, they did not remove all of the anti-Shiga agglutinins in absorption experiments. Modified lipid A core structure was detected in these hybrids, but Shiga O antigen was not expressed. When the his+ locus of the S. dysenteriae 1 chromosome was transferred by transduction to E. coli K-12 containing pWR24, complete Shiga O antigen was expressed. Lipopolysaccharide extracted from these hybrids was indistinguishable chemically, electrophoretically, and serologically from native S. dysenteriae 1 lipopolysaccharide.
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PMID:Expression of lipopolysaccharide O antigen in Escherichia coli K-12 hybrids containing plasmid and chromosomal genes from Shigella dysenteriae 1. 638 45


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