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

The phenol-phase soluble lipopolysaccharide isolated from Escherichia coli 0:157 by the hot phenol-water extraction procedure was shown by sodium dodecyl sulfate-polyacrylamide gel electrophoresis, periodate oxidation, methylation, and 13C and 1H nuclear magnetic resonance studies to be an unbranched linear polysaccharide with a tetrasaccharide repeating unit having the structure: (formula; see text) The serological cross-reactivity of E. coli 0:157 with Brucella abortus, Yersinia enterocolitica (serotype 0:9), group N Salmonella, and some other E. coli species can be related immunochemically to the presence of 1,2-glycosylated N-acylated 4-amino-4, 6-dideoxy-alpha-D-mannopyranosyl residues in the O-chains of their respective lipopolysaccharides.
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PMID:Structure of the O-chain polysaccharide of the phenol-phase soluble lipopolysaccharide of Escherichia coli 0:157:H7. 300 86

To determine whether lipopolysaccharide (LPS) structures of Campylobacter species are immunologically related to those of 11 other gram-negative organisms, we immunoblotted from polyacrylamide gels the LPS of these strains with immune rabbit serum raised against six Campylobacter jejuni strains and two Campylobacter fetus strains. The LPS studied were from Salmonella minnesota wild type and Ra to Re mutants, Salmonella typhi, Escherichia coli, Yersinia enterocolitica, Vibrio cholerae, and Pseudomonas aeruginosa. None of the 11 LPS preparations was recognized by the eight antisera, but antisera to each of the Campylobacter strains recognized core determinants of some LPS preparations. Antiserum directed against the most serum-sensitive C. jejuni strain, 79-193, was the only antiserum sample that recognized core regions of the rough Salmonella mutants. In converse experiments, when LPS preparations from five Campylobacter strains were blotted with antiserum to Salmonella lipid A, recognition of core structures of each was shown; data from an enzyme-linked immunosorbent assay confirmed this result. In contrast, antiserum to Salmonella typhimurium Re LPS showed no reactivity. We conclude that LPS of Campylobacter strains share lipid A antigenic determinants with the core region of LPS of several other gram-negative organisms.
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PMID:Lipopolysaccharide structures in Enterobacteriaceae, Pseudomonas aeruginosa, and Vibrio cholerae are immunologically related to Campylobacter spp. 307 30

The O-haptens of the major fraction (f5A) of B. abortus (Strains 2308 and 19) membrane bound smooth lipopolysaccharide (sLPS) were prepared by hydrolysis of f5A native sLPS in 1% acetic acid at 100 degrees C for 2 h. After hydrolysis, O-haptens were separated from Lipid A-protein complex by centrifugation, and from small fragments by ultrafiltration of molecular weight cut-off (MWCO) 1.0 X 10(3). These carbohydrate haptens were identified by precipitin-inhibition assay and further fractionated by both membrane filtration and dialysis. The size distributions of carbohydrate haptens of endotoxins (f5A) ranged from oligosaccharides up to polysacchandes of 1.0 X 10(4) MWCO. Three major fractions of MWCO 8.0-10.0 X 10(3), 3.5-5.0 X 10(3) and less than 1.0 X 10(3) from both strains 2308 and 19 contained more than 85% of the total immunoactive materials. These fractions of haptens were subjected to composition, proton and 13C NMR analysis and were found to be a homopolymer of alpha 1----2 linked, 4,5-dideoxy-4-formamido-D-mannose (N-formylperosamine), which is identical to O-haptens of B. abortus strain 119.3 and Yersinia enterocolitica serotype 0:9 and similar to Vibrio cholerae 569B (INABA). Fractions of these haptens exhibited similar inhibitory reactivities in a precipitin-inhibition assay as expressed as mumoles of monosaccharide of anhydro-N-formyl perosamine. They were about 480 times as active as Me alpha----DMan or DMan.
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PMID:Structural and immunochemical characterization of the O-haptens of Brucella abortus lipopolysaccharides from strains 19 and 2308. 311 17

Antisera were prepared in rabbits against formalized and heat-killed bacteria of Yersinia enterocolitica serotype O:5,27 and against formalized bacteria of serotype O:8. Both strains used for immunization demonstrated adhesion to and invasion of HeLa cells. Coating of the bacteria with antibody did not greatly alter adhesion (i.e., extracellular attachment) to HeLa cells; however, antibody against formalized bacteria of both serotypes inhibited HeLa cell invasion by the homologous and heterologous strains. The Fab fragments from purified immunoglobulins also demonstrated cross-reacting inhibition of HeLa cell invasion. Antibody against heat-killed bacteria of serotype O:5,27 had no inhibitory activity. Adsorption of the antiserum against formalized bacteria of serotype O:5,27 with lipopolysaccharide from the homologous strain removed anti-lipopolysaccharide antibody but did not remove the inhibitory activity. The antiserum against formalized bacteria of serotype O:8 showed no antibody against lipopolysaccharide from serotype O:5,27 and no agglutinins against heat-killed bacteria of this strain. From these results, it is tentatively suggested that protein structures are important in mediating epithelial cell invasion by Y. enterocolitica.
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PMID:Antibody inhibition of HeLa cell invasion by Yersinia enterocolitica. 313 17

Murine toxin of Yersinia pestis when injected in the rat tail vein (LD50) caused pronounced alterations in PGE1 and PGF2 alpha content in different tissues (lung, heart, spleen, liver, kidney, small intestine) and blood. Heat-inactivated toxin has been shown to have the same effects as the intact toxin preparation. The changes in PG content are, probably, due to the lipopolysaccharide component of both preparations. The differences in metabolic effects between Yersinia pestis endotoxin and lipopolysaccharides of other Gram-negative bacteria are discussed.
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PMID:[Levels of prostaglandin E1 and F2 alpha in the dynamics of toxic-infectious shock induced by Yersinia pestis]. 316 86

Eighteen monoclonal antibodies were generated from mice immunized with Vibrio cholerae O1 serotype Inaba. Reactivities of these antibodies were investigated by slide agglutination, microdilution agglutination, and passive hemagglutination tests. Although all antibodies reacted to the Inaba-type cells, reactivity to Ogawa cells showed some variation. These antibodies were roughly subdivided into three groups by slide agglutination tests and microdilution agglutination tests by using type-specific standard strains. The first group showed almost identical reactivities to both the Ogawa- and the Inaba-type cells, while the second group reacted to Inaba-type cells but only very weakly reacted to Ogawa-type cells. The third group reacted only to Inaba-type cells; no agglutination was observed for Ogawa-type cells in either the slide agglutination or the microdilution agglutination tests. Most of the third group showed cross-reactivity to Brucella abortus and Yersinia enterocolitica O9. Results of passive hemagglutination tests showed that all 18 antibodies were to the lipopolysaccharide of V. cholerae O1.
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PMID:Monoclonal antibodies to Vibrio cholerae O1 serotype inaba. 323 65

Rat ankle joints injected intraarticularly with 5 micrograms of group A streptococcal peptidoglycan-polysaccharide (PG-APS) developed an acute course of arthritis. Recurrence of arthritis was induced in 100% of these joints by intravenous injection of as little as 10 micrograms of Salmonella typhimurium lipopolysaccharide (LPS) 3 wk after intraarticular injection. This reaction was similar in athymic and euthymic rats. Buffalo rats were less susceptible than Lewis or Sprague-Dawley rats. Neisseria gonorrhoeae, Yersinia enterocolitica, and Escherichia coli LPS, and S. typhimurium Re mutant LPS, were also active. Re mutant LPS activity was greatly reduced by mixing with polymyxin B. E. coli lipid A was weakly active. An acute synovitis of much less incidence, severity, and duration was seen in contralateral joints injected initially with saline, and in ankle joints of naive, previously uninjected rats after intravenous LPS injection. The intravenous injection of the muramidase mutanolysin on day 0 or 7 after intraarticular PG-APS injection prevented LPS-induced recurrence of arthritis. These studies suggest that the phlogistic activities of lipid A and peptidoglycan might interact in an inflammatory disease process, and that LPS may play a role in recurrent episodes of rheumatoid arthritis or reactive arthritis.
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PMID:Lipopolysaccharide induces recurrence of arthritis in rat joints previously injured by peptidoglycan-polysaccharide. 329 8

The porin proteins of Escherichia coli, Yersinia enterocolitica, and Salmonella minnesota were found to co-extract by the phenol-chloroform-petroleum ether method together with the R lipopolysaccharide of these strains. Lipopolysaccharide free protein recovered from the phenolic residue of the phenol-chloroform-petroleum ether extract migrated as a Mr 36-37,000 protein. We could demonstrate that the protein was extracted from bacteria as a high molecular weight protein-lipopolysaccharide complex. Once exposed to phenolic conditions, the protein was no longer soluble in the phenol-chloroform-petroleum ether extraction mixture, indicating a highly specific lipopolysaccharide-protein association.
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PMID:Characterisation of protein co-extracted together with LPS in Escherichia coli, Salmonella minnesota and Yersinia enterocolitica. 333 95

By means of quantitative immuno-electrophoretic methods, 81 different antigens were demonstrated in sonicated preparations of Yersinia enterocolitica, serogroup 0:3, using corresponding rabbit antiserum. Only chromosomally-encoded antigens were demonstrated in this system. Thirteen antigens were located on the bacterial surface, as demonstrated after absorption of rabbit antiserum with whole, killed bacteria. Five antigens resisted boiling. Antigen No. 71 was identified as an important part of the lipopolysaccharide, and antigen No. 6 as the "common antigen" of Pseudomonas aeruginosa. Binding activities to concanavalin A (indicating the presence of carbohydrates), to Limulus amoebocyte lysate and to polymyxin B (indicating the presence of possible endotoxin activity) were demonstrated for five, nine, and seven antigens, respectively. These observations, together with the presence of corresponding antibodies in pre-immune rabbit sera, as well as cross-reactivity with other Gram-negative bacteria, indicate the biological importance of several of these antigens.
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PMID:Crossed immuno-electrophoretic analysis of Yersinia enterocolitica serotype 0:3 antigens. 337 Jan 55

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


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