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

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

A novel transposon mutagenesis system has been developed for Shigella. We have used it to isolate specific mutants of Shigella sonnei and Shigella dysenteriae 1 that fail to produce lipopolysaccharide 'O' side chains. The virulence of the mutants was evaluated in the Sereny test and in a HeLa cell invasion assay. All HO'-minus mutants failed to provoke a positive Sereny reaction but retained the ability to invade HeLa cells. This demonstrates that 'O' side chains are virulence factors of S. sonnei and S. dysenteriae 1. 'O'-minus mutants of S. sonnei which still contained the Form I plasmid were capable of invading HeLa cells whilst plasmid-minus mutants were not, demonstrating that this plasmid encodes properties other than 'O'-antigen production that are involved in virulence.
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PMID:'O'-antigens are essential virulence factors of Shigella sonnei and Shigella dysenteriae 1. 241 50

Immunoglobulin G3 murine monoclonal antibody T6 specific for the lipopolysaccharide of Salmonella O serogroups A to E was established. By using R mutants of Salmonella spp., Escherichia coli, and Shigella spp., the major reactive epitope with T6 was tentatively identified as the terminal disaccharide, N-acetylglucosamine 1.2----alpha glucose, of the core oligosaccharide. T6 was reactive with 10 clinical isolates of each of the Salmonella O serogroups A to E but not with 58 isolates of other gram-negative bacteria. Its selective reactivity against Salmonella spp. renders T6 a potentially more useful reagent than the conventional polyvalent serum for the identification of Salmonella spp. It may also serve as a useful molecular tool for the study of the outer core structure of all Salmonella and related species.
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PMID:A murine monoclonal antibody specific for the outer core oligosaccharide of Salmonella lipopolysaccharide. 243 13

It is well established that plasmids are involved in the expression of lipopolysaccharide in certain species of Shigella. In Shigella sonnei, both the biosynthesis of oligosaccharide side chains (O antigen), and cell invasiveness are controlled exclusively by a 120 megadalton (MDa) plasmid. In Shigella dysenteriae 1, a 10 kilobase (kb) plasmid is required for O-antigen production. Shigella dysenteriae 1 strains devoid of this plasmid lose the ability to synthesize O antigen. Interestingly, this 10-kb plasmid is not stably maintained in Escherichia coli K-12 strains, where it is lost spontaneously at a high frequency. Our genetic analyses of Shigella dysenteriae 1 strain IDBM11 and its derivatives indicate that the stability of this plasmid is associated with the histidine region of the chromosome which is unique to Shigella dysenteriae. Furthermore, the 10-kb plasmid is stably maintained in wild-type IDBM11 with an intact histidine locus. However, this plasmid is not stable in IDBM11 derivatives (e.g., IDBM11-1 and IDBM11-2), in which the his locus has been substituted with the histidine region of an E. coli K-12 chromosome. The S. dysenteriae IDBM11 strain, and its derivatives (lacking a 10-kb plasmid), displayed an invasive property as demonstrated by their internalization by HeLa cells in an in vitro assay. Thus the 10-kb plasmid of Shigella dysenteriae 1 is required for O-antigen synthesis but not for cell invasion.
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PMID:The stability of O-antigen plasmid is determined by a chromosomal region of Shigella dysenteriae 1. 245 51

The experiment was made on 16 monkeys (rhesus macaques). Only 1 out of 12 monkeys immunized with S. sonnei ribosomal vaccine and all 4 control monkeys fell ill as the result of oral challenge with S. sonnei virulent strain. The immunized monkeys stopped excreting Shigellae earlier than the control monkeys. Antibody to lipopolysaccharide (LPS) in the serum and saliva of the monkeys were studied in the enzyme immunoassay with monospecific antibodies to human IgA, IgG and IgM. A single injection of the ribosomal vaccine in a dose of 600 micrograms was shown to lead to a considerable increase in the levels of IgA, IgG and IgM antibodies to LPS in saliva. In parenteral immunization with the ribosomal vaccine the stimulation of secretory IgA system is similar to that resulting from oral challenge with Shigella virulent strain introduced in a dose of 50 X 10(9) microbial cells. No difference in the response of monkeys to primary and booster immunization was noted.
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PMID:[Stimulation of the secretory IgA system in monkeys by parenteral immunization with a ribosomal Sonne dysentery vaccine]. 246 72

Achieving a vigorous secretory immunoglobulin A (IgA) response in intestinal secretions usually requires multiple doses of antigen given orally, while systemic immunity is more easily attained by parenteral immunization. This study examines the role of combined parenteral and oral immunizations to enhance the early mucosal immune response to an enteropathogen. We have used a chronically isolated intestinal-loop model in rabbits as a probe to monitor kinetically the initial (primary) local immune response to shigella lipopolysaccharide (LPS) following combinations of parenteral immunization intramuscularly (i.m.) and oral stimulation with shigellae. Predictably, effective stimulation of systemic immunity was elicited when heat-killed preparations of Shigella sp. strain X16 were given i.m., as shown by strong serum IgG and weak intestinal IgA activity to shigella LPS. A single oral dose of live Shigella sp. strain X16 given to unprimed rabbits elicited only a typical weak IgA response in intestinal secretions. However, when an i.m. dose of heat-killed shigellae was followed 1 day later by an oral dose of live Shigella sp. strain X16, a hyperstimulation of the early secretory IgA response was elicited, and the response reached levels found previously only after multiple oral administrations of live shigellae. This stimulation did not require the use of an adjuvant. At the same time, the animals receiving this combined oral and i.m. regimen had a lower IgG antishigella LPS activity in serum compared with their response after receiving parenteral antigen in adjuvant alone. These findings indicate that while a dichotomy exists between the systemic and mucosal immune responses, careful orchestration of the stimulatory events can promote a vigorous early local IgA response.
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PMID:Combined parenteral and oral immunization results in an enhanced mucosal immunoglobulin A response to Shigella flexneri. 327 85

The role of a plasmid in the virulence activity of an enteropathogenic Escherichia coli (EPEC) strain belonging to serotype 0111:NM was examined. EPEC strain B171, which is resistant to chloramphenicol, streptomycin, sulfathiazole, and tetracycline, harbors a 54-megadalton plasmid, pYR111, and exhibits localized adherence (LA) with HeLa cells. Curing the plasmid yielded strain B171-4, which had lost the ability to exhibit LA, resistance to the antibiotics, and the lipopolysaccharide (LPS) O-antigenic polysaccharide. To confirm that these phenotypic characteristics were specified by pYR111, the plasmid was transferred by conjugation into a nalidixic acid-resistant strain of E. coli HB101. LA and antimicrobial resistance were expressed in most of the transconjugants examined. The O-polysaccharide side chains, antigenically reactive with O111-specific antiserum, were also expressed by the transconjugants. Although EPEC plasmids coding for both drug resistance and LA have been described, an EPEC plasmid encoding the expression of an LPS O antigen has not been previously reported. Similar findings described for some Shigella and Salmonella strains suggest that plasmid-encoded modification of the LPS in some enteric bacterial species may be more common than previously recognized and may contribute to the characteristic virulence activity of the organism.
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PMID:Plasmid-encoded expression of lipopolysaccharide O-antigenic polysaccharide in enteropathogenic Escherichia coli. 330 60

1. Smooth to rough mutation has the same biochemical basis in Shigella as in Salmonella. It is the result of enzyme defects blocking the incorporation of the O-specific side chains that characterize the smooth lipopolysaccharide with the consequent exposure of the underlying basal structures that determine ;rough'-specificity. 2. The Shigella flexneri basal structure resembles its Salmonella analogue in that it has the same qualitative sugar composition, and enzyme defects in its biosynthetic pathway give rise to ;rough'-lipopolysaccharides that are indistinguishable from those of Salmonella chemotypes Ra, Rb, Rc and Rd. However, the Salmonella and Shigella basal structures are not identical as judged by quantitative analysis and the absence of serological cross-reaction. 3. The Sh. flexneri basal structure side chain has been isolated and characterized as an alpha-N-acetylglucosaminyl-(1-->4)-galactosyl-(1-->3)-glucose sequence with alpha-glucosyl radicals substituted on the 3- and 4-positions of the galactose and glucose respectively. The different sugar types in this side chain are incorporated into the growing molecule in the same order as in Salmonella, which explains why the enzyme defects associated with smooth to rough mutation produce the same series of R-chemotypes from both genera. The terminal alpha-glucosyl and alpha-N-acetylglucosaminyl-(1-->4)-galactosyl residues of the Sh. flexneri basal structure are sufficiently different from the terminal alpha-galactosyl and alpha-N-acetylglucosaminylglucosyl residues of the Salmonella analogue that they offer an explanation for the absence of serological cross-reaction between these two basal structures.
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PMID:The immunochemistry of Shigella flexneri O-antigens. The biochemical basis of smooth to rough mutation. 606 Apr 53

Many rough mutants selected from isogenic smooth virulent and avirulent strains of Shigella flexneri were examined for virulence, using tissue culture infection and Sereny tests. Many of the rough mutants isolated from a virulent smooth strain were capable of penetrating tissue culture cells but incapable of producing a positive Sereny test. In contrast, we could not obtain from smooth avirulent strains any rough mutants capable of penetrating HeLa cells. Chemical analysis of lipopolysaccharide of some representative rough strains showed several patterns of sugar composition with a range of from Ra to Re chemotypes. There was no correlation between HeLa cell invasiveness and chemotypes of lipopolysaccharides, thus indicating little significance of oligosaccharides of the rough core as well as O antigens in the ability of S. flexneri to penetrate HeLa cells. When these invasive rough strains were given O antigen genes from a smooth avirulent Shigella Hfr strain, most of the transconjugants that expressed O antigens regained the ability to evoke keratoconjunctivitis in guinea pigs. We also examined the chromosomal loci of HeLa cell invasion by transferring carbohydrate fermentation genes of Escherichia coli K-12 Hfr and found two chromosomal loci, the rha and lac-gal regions, which control the ability to penetrate HeLa cells. These results suggested that O antigens and ability to penetrate tissue culture cells are independent and prerequisite attributes of virulence in Shigella flexneri to evoke keratoconjunctivitis in guinea pigs.
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PMID:HeLa cell invasiveness and O antigen of Shigella flexneri as separate and prerequisite attributes of virulence to evoke keratoconjunctivitis in guinea pigs. 618 81

Salmonella typhi 5076-1C, a potential live, oral vaccine for protection against typhoid fever and Shigella sonnei shigellosis, expresses the S. sonnei form I antigen and normal S. typhi somatic antigens. Polysaccharide antigens of this galactose epimeraseless genetic derivative strain were hot phenol-water extracted from cells grown with (+gal) and without (-gal) galactose. Ultracentrifugation of the aqueous layer from (+gal) cells resulted in a lipopolysaccharide (LPS) pellet having core-linked S. typhi O-antigen but no core-linked form I antigen; the LPS from (-gal) cells lacked O-antigen. The form I antigen, obtained from the supernatant, was purified by alcohol precipitation and ion exchange chromatography. Unlinked form I and S. typhi O-polysaccharide antigens, both present in the (+gal) supernatant, were further separated by gel filtration. Chemical analyses revealed the 5076-1C form I antigen to be a polymer (Mr = 14,000-20,000) having O-disaccharide repeating units comprised of 2-acetamido-4-amino-2, 4,6-trideoxy-D-galactose and 2-acetamido-2-deoxy-L-altruronic acid. Unlike parental S. sonnei form I LPS, the 5076-1C form I antigen lacked core lipid A, had low phosphorus content, and migrated in polyacrylamide gels with lower relative mobility. In contrast to current concepts of LPS assembly, these data indicate that 5076-1C form I antigen is transported to the cell surface without covalent linkage to core lipid A, and exists as a polymerized, antigenic surface entity.
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PMID:Unusual lipopolysaccharide antigens of a Salmonella typhi oral vaccine strain expressing the Shigella sonnei form I antigen. 637 5


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