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

The chemical structure of the O-antigen of a proposed new provisional serotype of Shigella flexneri has been determined. Methylation analysis, GLC-MS, 1H-NMR and 13C-NMR showed that the linear O-antigenic polysaccharide is the same as for all S. flexneri [Kenne, L., Lindberg, B., Petersson, K. & Romanowska, E. (1977) Carbohydr. Res. 56, 363-370]. A novel structural feature is that the disaccharide alpha-D-Glcp-(1----2)-alpha-D-Glcp is linked to O4 of the N-acetyl-glucosamine residue. (Formula: see text) Western blotting of the lipopolysaccharide with an E. coli R3 core-specific monoclonal antibody, suggested the presence of an E. coli R3 core.
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PMID:Structural and immunochemical studies of the lipopolysaccharide from a new provisional serotype of Shigella flexneri. 245 60

A panel of 10 mouse and rat monoclonal antibodies specific for different type- and group-specific O-antigenic determinants of Shigella flexneri lipopolysaccharide was used to serotype 240 isolates of S. flexneri from Bangladesh. Three immunoglobulin M antibodies were used in a direct slide agglutination test; seven immunoglobulin G antibodies were absorbed to Staphylococcus aureus and used in a coagglutination assay. All but 13 of the isolates could be serotyped by using the monclonal antibodies. The six most common serotypes were (in descending order) 2a, 2b, Y (E1037), 1a, 3a, and 1b and accounted for more than 80% of all isolates. Two of the nontypable strains were found to be of a new provisional serotype of S. flexneri (T. Wehler and N.I.A. Carlin, Eur. J. Biochem. 176:471-476, 1988). The 11 remaining strains were found to be rough and therefore nontypable. The serotyping scheme based on the panel of monoclonal antibodies is specific and holds the potential to be developed into a useful tool for epidemiological investigation. The study also demonstrates that the recently described E1037 antigen is commonly found among at least four serotypes (4a, 6, X, and Y) of S. flexneri.
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PMID:Use of monoclonal antibodies to type Shigella flexneri in Bangladesh. 266 35

Preincubation of human umbilical vein endothelial cell (EC) monolayers with 1 ng to 10 micrograms/ml lipopolysaccharide (LPS) increased the binding of T lymphocytes to EC. The effect was maximal at LPS concentrations of 0.1 to 10 micrograms/ml, and occurred with LPS derived from Escherichia coli (serotypes 0111:B4 and 0127:B8), Shigella flexneri (serotype 2a), Serratia marcescens (serotype 0:3), and Yersinia entercolitica (serotype 0:3). The increased binding appeared to be mediated primarily through an action on EC; preincubation of T cells rather than EC with LPS did not lead to enhanced binding. The onset of enhanced binding was very rapid, being observed after 2 to 3 min of preincubation and becoming maximal after 1 hr. EC were unresponsive to LPS after fixation with 2% paraformaldehyde-L-lysine-periodate and also when the LPS was incubated with EC at 4 degrees C. Enhanced binding was seen with lipid A and with LPS from Salmonella minnesota Re 595 (mainly lipid A) and was abolished by conjugation with polymyxin B. The observed increase in the binding of lymphocytes to EC exposed to LPS suggests that the lymphocytopenia induced by endotoxemia may result from augmentation of the adherence of lymphocytes to altered endothelium.
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PMID:Effects of bacterial lipopolysaccharide on the binding of lymphocytes to endothelial cell monolayers. 348 95

The subclass distribution of human serum antibodies to the O-antigenic lipopolysaccharides of Salmonella serogroups B and D and to Shigella flexneri serotypes 1b, 2a, and 4a lipopolysaccharide antigens were analyzed in an enzyme-linked immunosorbent assay with monoclonal antibodies to the immunoglobulin subclasses. The patients had culture-verified Salmonella (17 Swedes) or Shigella flexneri (23 Vietnamese; 11 children and 12 adults) infections. Consecutive samples drawn during 1 year postinfection were investigated. Antibodies to the Salmonella antigens were mainly of the immunoglobulin G1 (IgG1), IgA1, and IgA2 subclasses. For the Salmonella serogroup B O polysaccharide, the IgA1 and IgA2 subclasses had peak values earlier than (6/9) or coinciding with the IgG1 (3/9) peak value. Furthermore, the IgA2 response to Salmonella serogroup B was positively correlated to the duration of the carrier state (P less than 0.001); the corresponding IgA1 response was less well correlated but was still significant (P less than 0.02). In the case of the Shigella flexneri O polysaccharide, specific antibodies appeared mainly in the IgG1 and IgA1 subclasses. Some IgG2 was also found, surprisingly even in very young patients. No subclass shift with time within the immunoglobulin classes was noted in any of the groups.
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PMID:Immunoglobulin G (IgG) and IgA subclass pattern of human antibodies to Shigella flexneri and Salmonella serogroup B and D lipopolysaccharide O antigens. 351 61

Anti-lipopolysaccharide equine hyperimmune plasma (anti-LPS), which has been used successfully to treat LPS (endotoxin)-mediated disorders, has been further characterised. IgG present in anti-LPS had the highest affinity for LPS prepared from Salmonella typhimurium, S. typhi, S. abortus equi and Shigella flexneri and intermediate affinity for Escherichia coli O55:B5, E. coli O127:B8 and S. enteritidis. Anti-LPS destroyed by means of complement activation a wide range of gram-negative bacteria, including various species and strains of Klebsiella, Enterobacter, E. coli, Sh. flexneri, Providencia, Salmonella and Pseudomonas. Control plasmas or saline had little or no effect. Maximum killing occurred within seconds to minutes. Electronmicroscopy showed that anti-LPS treatment of K. pneumoniae caused extensive cell wall and cytoplastic membrane disruption, followed by the appearance of spheroplasts and cell ghosts. Antibodies were required in 100,000-fold excess to inhibit the limulus amoebocyte lysate reaction with LPS from E. coli. Anti-LPS thus contains IgG that binds to a wide range of LPS, and can destroy a wide range of gram-negative bacteria by means of complement activation.
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PMID:Properties of equine anti-lipopolysaccharide hyperimmune plasma: binding to lipopolysaccharide and bactericidal activity against gram-negative bacteria. 366 52

Blood donated to the Natal Blood Transfusion Service was screened by an enzyme-linked immunosorbent assay (ELISA) for anti-lipopolysaccharide (anti-LPS) antibodies. Plasma units with high concentrations (greater than 40 micrograms/ml) of anti-LPS IgG were pooled and fractionated to obtain a gamma globulin (lot LG-1). The binding of LG-1 antibodies to LPS prepared from 14 bacterial species and strains was found to be the highest to LPS from Shigella flexneri, Salmonella abortus equi and Salmonella typhimurium and intermediate with Klebsiella pneumoniae, Pseudomonas aeruginosa, Salmonella enteritidis and Escherichia coli 026:B6. Differential absorption experiments showed that LG-1 contained a mixture of specific and cross-reacting antibodies. A large proportion of antibodies binding to Sh. flexneri LPS were mainly specific, while those binding to S. typhimurium and the other Salmonella species tested were largely cross-reactive. There was little correlation between the spectrum of activity of the LG-1 antibodies and the incidence of gram-negative bacteria in blood cultures taken from hospital patients in an area covered by the Transfusion Service. Mice treated with LG-1 prior to inoculation with P. aeruginosa were significantly protected against morbidity and mortality compared to controls.
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PMID:Properties of human anti-lipopolysaccharide gamma globulin: specificity and protective effects. 392 17

The insensitivity of wild-type Shigella flexneri 2a to coliphage lambda is a consequence of its native genetic defect in the malA gene cluster. The "smooth" S. flexneri 2a lipopolysaccharide layer affects the efficient adsorption of lambda. Derivatives, capable of serving as functional hosts for lambda, were obtained by repairing the malA lesion, enabling the expression of the malB-lambdarcp region of S. flexneri. Introduction of a mutation into S. flexneri causing a "rough" lipopolysaccharide character resulted in more efficient adsorption of lambda. Such S. flexneri hosts can be stably lysogenized and upon induction yield gal(+)-transducing lysates. Lambda propagated on a malA(+) rough S. flexneri host was restricted by Escherichia coli K-12 and E. coli B, but not by E. coli C. This S. flexneri host did not restrict lambda grown on these E. coli strains.
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PMID:Behavior of coliphage lambda in Shigella flexneri 2a. 1456 94

An avirulent mutant of Shigella flexneri 2a, when grown in broth containing calcium ions, was found to have a three- to fourfold increase in electrophoretic mobility toward the anode when compared to its virulent parent. Under these same growth conditions, it was found that the avirulent strain was made more electronegative in the presence of ethylenediaminetetraacetic acid (EDTA). EDTA had no effect on the electrophoretic mobility of the virulent strain. In the absence of added calcium in the growth medium, no differences between the strains were observed. The alteration which has resulted in an increased negative charge has also stabilized the avirulent strain against loss of lipopolysaccharide from EDTA treatment.
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PMID:Mutation in Shigella flexneri 2a resulting in increased electrophoretic mobility. 462 53

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


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