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

Aqueous biphasic partitioning of Salmonella typhimurium S and R bacteria in a system containing 6.2 per cent (w/w) dextran 500 and 4.4 per cent (w/w) poly(ethyleneglycol) 6000 (PEG) was similar to the partition of the corresponding surface lipopolysaccharide (LPS). Further partition analysis with charged PEG showed that S bacteria and their LPS exposed very little charge, whereas R bacteria and their LPS showed a conspicuous negative charge at neutral pH. Free zone electrophoresis also indicated that the S bacteria have a much lower surface charge density than the R bacteria and accordingly a different surface structure. Thus, the physico-chemical properties of the bacterial surface seem to be determined to a great extent by the characteristics of the cell surface LPS.
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PMID:Surface-charge characteristics of smooth and rough Salmonella typhimurium bacteria determined by aqueous two-phase partitioning and free zones electrophoresis. 2 49

Oral dosing of adult male F344 rats with the glycol ether 2-methoxyethanol (ME) or its principal metabolite 2-methoxyacetic acid (MAA) results in the suppression of the primary plaque-forming cell (PFC) response to trinitrophenyl-lipopolysaccharide (TNP-LPS). In the present study, the PFC response to TNP-LPS was used to evaluate the immunotoxic potential of ethylene glycol (EG) as well as the glycol ethers 2-methoxyethyl acetate (MEA), 2-(2-methoxyethoxy) ethanol, bis(2-methoxyethyl) ether, 2-ethoxyethanol and its principal metabolite 2-ethoxyacetic acid, 2-ethoxyethyl acetate, and 2-butoxyethanol relative to ME and MAA. Rats were immunized with TNP-LPS and then exposed 4 and 28 hr later to 50, 100, 200, or 400 mg/kg of glycol ether or EG. Three days following immunization, the PFC response to TNP-LPS was determined. In addition to ME and MAA, only MEA, which was as effective as ME, suppressed the PFC response to TNP-LPS. Concomitant administration of the alcohol dehydrogenase inhibitor 4-methylpyrazole with ME or MEA prevented suppression of the PFC response by these glycol ethers. These results indicate that of the chemicals tested only ME, MEA, and MAA are immunosuppressive, and that oxidative metabolism via alcohol dehydrogenase is necessary for ME- and MEA-suppression of the response to TNP-LPS.
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PMID:Comparative immunosuppression of various glycol ethers orally administered to Fischer 344 rats. 152 76

Sputum samples from seven patients with cystic fibrosis and chronic P. aeruginosa lung infection were investigated for immune complexes by PEG precipitation and in two different complement binding assays. All seven patients were immune complex positive. The components involved in immune complex formation were identified by SDS-PAGE and immunoblotting. We found P. aeruginosa lipopolysaccharide as a major antigen. Both core and O-specific saccharide antigens could be demonstrated. IgG and IgA were the immunoglobulins involved, with IgG2 as the dominating IgG subclass. Lipopolysaccharide has a number of biological activities and its presence in sputum may have consequences for the pathogenesis of lung disease in cystic fibrosis.
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PMID:Lipopolysaccharide is present in immune complexes isolated from sputum in patients with cystic fibrosis and chronic Pseudomonas aeruginosa lung infection. 155 93

Macrophage cytocidal activation requires the sequential impingement on the macrophage of a priming stimulus (interferon [IFN] alpha, beta, or gamma) and a triggering stimulus (such as polyinosinic acid:polycytidylic acid [poly [I:C]] or bacterial lipopolysaccharide). The mechanism of progression from the IFN-primed state to the cytocidal state is poorly understood. By quantifying the level of expression of a gene product (complement component factor B [Bf]) associated with cytocidal activation and through the use of phenotypically distinct populations of macrophages (unprimed and IFN-primed), we have investigated the functional necessity of changes in intracellular concentration of free calcium ions ([Ca2+]i) in signaling the transition from the primed to the cytocidal state. Elevating the [Ca2+]i by incubation of unprimed macrophages with the calcium ionophore, ionomycin, failed to induce the expression of Bf. By contrast, Bf was expressed at high levels when IFN-primed macrophages were exposed to ionomycin, suggesting that priming induced within the macrophages the capacity to respond to a nonspecific change in [Ca2+]i. Quantification of the [Ca2+]i in response to exposure to ionomycin revealed an initial transient elevation, followed by a secondary sustained component. No differences in these changes were observed between unprimed and IFN-primed macrophages. We therefore questioned if changes in [Ca2+]i were also implicated in the transition between the primed and the cytocidal state using the ligand, poly [I:C]. In contrast to ionomycin, incubation of IFN-primed macrophages with poly [I:C] did not sustain measurable increases in [Ca2+]i, yet fully stimulated the transition from the IFN primed to the cytocidal state. However, incubation of IFN-primed macrophages with poly [I:C] in the presence of 1) a Ca2+/ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid buffer calculated to clamp the extracellular concentration of free calcium ions to a value approximately equal to the resting [Ca2+]i; 2) the calcium channel blocker verapamil; or 3) the intracellular Ca2+ antagonists (W-7, W-13, and TMB-8) substantially inhibited the induction of Bf. Collectively, these data support the following conclusions. First, that changes in [Ca2+]i comprise an important element in the induction of progression from the IFN-primed to the cytocidal state. Second, the failure to detect global changes in [Ca2+]i in response to the ligand, poly [I:C], suggests that changes in [Ca2+]i or Ca2+ movement may occur in either a spatially restricted or in an asynchronous cyclical fashion and are not detected by population fluorescence measurements. Third, the source of the relevant Ca2+ is extracellular. Fourth, our findings suggest that priming influences macrophage functional responses at a locus that is distal to the changes in [Ca2+]i, thereby potentially allowing signaling processes to be utilized to initiate different cellular responses.
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PMID:Transmembrane-mediated changes in [Ca2+] are involved in the signaling pathway leading to macrophage cytocidal differentiation: implications of localized changes in intracellular [Ca2+] and of interferon priming on Ca2+ utilization. 162 33

Mononuclear phagocyte activation is characterized by alterations in cellular metabolism and plasma membrane composition. In rodent and human systems, antibodies (conventional heteroantibodies or monoclonal reagents) that identify plasma membrane antigens selectively expressed by activated macrophages and monocytes have been generated. Among these activation-associated determinants is Mo3e (p50,80), a protease-sensitive antigen that is expressed by human monocytes activated in culture by exposure to bacterial lipopolysaccharide, muramyl dipeptide, or phorbol myristate acetate (PMA) (as well as other biologically active phorbol compounds). Mo3e is also expressed by the monoblastic cell line U-937 after culture in medium containing PMA and other pharmacological activators of protein kinase C (4 beta-phorbol-12,13-dibutyrate, 4 beta-phorbol-12,13-didecanoate, mezerein, and cell-permeable 1,2-diacylglycerol). The human promyelocytic cell line HL-60 becomes Mo3e positive after exposure in vitro to certain inducers of monocytic differentiation (PMA, dibutyryl cyclic AMP, and cholera toxin plus 3-isobutyl-1-methylxanthine). The surface expression of Mo3e is blocked by inhibitors of protein synthesis, N-linked glycosylation, and protein kinase activation, as well as by ethylene glycol bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid and calcium antagonists. These data suggest the involvement of glycoprotein synthesis, protein kinase activation, and calcium ions in the stimulated expression of Mo3e by activated human mononuclear phagocytes. Anti-Mo3e antibody blocks the human monocyte response to migration inhibitory factor (MIF), which indicates an association between the expression of Mo3e antigen and responsiveness to MIF.
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PMID:Mononuclear phagocyte activation: activation-associated antigens. 242 78

Surface proteins of nine Campylobacter jejuni strains belonging to three different serovia were extracted with lysozyme/ethylenediamine-tetraacetic acid. The preparations bound to isolated murine small intestinal cells and to a membrane fraction (MF) of isolated brush borders obtained by detergent treatment with Triton X-100 and Nonidet P40. Binding was demonstrated by an enzyme-linked immunosorbent assay procedure. Using lipopolysaccharide (LPS)- and flagella-specific antisera the contribution of flagella and LPS, present in the protein preparations, to the total binding to MF was investigated. Only up to approximately 10% of the total binding of each strain was found to be mediated by LPS, 10%-33% of binding was flagella dependent. The preparations of four strains (serovar HS2) bound in a trypsin-sensitive manner (45%-85% reduction), while the others (serovaria HS1 and HS13) were hardly influenced by trypsin treatment. Binding to MF was not impaired by preincubation of the bacterial surface protein preparations with several sugars and lectins.
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PMID:In vitro binding of Campylobacter jejuni surface proteins to murine small intestinal cell membranes. 274 90

Studies of the serum bactericidal system in bovine brucellosis were undertaken to investigate the role of the humoral immune response in protection of cattle against the facultative intracellular parasite Brucella abortus. Fresh sera from normal control cattle, infected cattle, and cattle immunized with B. abortus cell envelopes were collected before treatment and during the course of immunization or infection. Normal fresh bovine serum or fresh agammaglobulinemic serum from colostrum-deprived calves was effective in killing smooth virulent B. abortus 2308, but rough strains RB51 (a rough mutant of strain 2308) and 45/20 were much more sensitive to serum. The difference in susceptibility to serum was shown to be correlated with differences in lipopolysaccharide chemotype, with the more resistant strain 2308 having O polysaccharide and the more susceptible strains 45/20 and RB51 lacking O side chains. By treatment of fresh serum with MgCl2 and EGTA [ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid] killing was shown to occur via the classical pathway of complement activation. When antibody to B. abortus was present, killing of strain RB51 increased but killing of smooth strain 2308 decreased. The earliest antibody response in serum from infected animals did not interfere with killing. When affinity-purified bovine immunoglobulins specific for B. abortus smooth lipopolysaccharide were added to fresh normal bovine serum, immunoglobulin G1 (IgG1) and IgG2 isotypes blocked killing but IgM and IgA isotypes did not. Thus, it appears that serum from previously unexposed animals or animals early during infection can kill smooth B. abortus, an appropriate defense mechanism before the organism becomes intracellular. At later stages of infection, blocking antibodies predominate.
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PMID:Killing of Brucella abortus by bovine serum. 314 Dec 87

Enteropathogenic Yersinia sp. releases plasmid-associated proteins of low molecular mass (26-67 kilodaltons) at 37 degrees C. In this study, the optimum conditions for the release of proteins were assessed and the released proteins (RPs) were analyzed for the manner of release, immunochemical characteristics, and the location of the genes necessary for their synthesis. Protein release was strongly enhanced when growth media were markedly depleted of calcium ions by precipitation with oxalate or chelation with EGTA [ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid]. RP yields were greatest when Yersinia spp. were in the exponential growth phase. The RPs appeared to be released from the Yersinia spp. by secretion rather than by pinching off of membrane vesicles, because the RPs did not sediment during high-speed centrifugation nor were they contaminated to any significant degree with lipopolysaccharide. Moreover, immunoblot analysis revealed only traces of protein species related to RPs within the outer membranes of plasmid-positive Yersinia spp. grown at 37 degrees C under calcium-restricted conditions. Immunoblot studies also showed that the RPs of Y. enterocolitica serotypes O:3, O:8, and O:9 and the RP of Y. pseudotuberculosis serotype I are highly cross-reactive. Finally, the immunoprecipitates of the products of minicells which harbor Yersinia plasmids were used to demonstrate that at least three proteins immunochemically related to the released fraction were plasmid encoded. These results suggest that at least three of the RPs may be related to or identical with previously described plasmid-encoded Yersinia outer membrane proteins.
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PMID:Immunochemical analysis of plasmid-encoded proteins released by enteropathogenic Yersinia sp. grown in calcium-deficient media. 377 Sep 52

The role of lipopolysaccharide (LPS) in the susceptibility of Haemophilus ducreyi to human serum and the mechanism of complement activation by serum-susceptible (Sers) strains were investigated. Serum treated with 2 mM Mg2+ and 20 mM ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid was nonbactericidal, but inulin-treated serum remained bactericidal. Absorption of serum with heat-killed whole cells of an Sers strain removed its bactericidal activity against the absorbing strain and also against other Sers strains. LPS obtained from Sers strains inhibited the bactericidal activity of serum against all Sers strains, whereas LPS from serum-resistant (Serr) strains and an Serr isogenic strain did not. However, high concentrations of LPS from the Serr strain inhibited the bactericidal activity of serum, an indication that part of the structural site involved in serum susceptibility is retained in the LPS of this strain. The LPS of Sers strains exhibited higher anticomplement activity than the LPS of Serr strains. These findings suggest that the classical pathway of complement activation is involved in the serum killing of H. ducreyi and that LPS composition may contribute to their susceptibility to complement-mediated serum bactericidal activity.
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PMID:Role of lipopolysaccharide and complement in susceptibility of Haemophilus ducreyi to human serum. 387 95

The contact angles on cell layers of a series of polymeric droplets from aqueous two-phase systems of dextran and poly(ethylene glycol) have been used to determine the critical or limiting interfacial tension for spreading on the cell layers. Test droplets of the denser dextran-rich phase were formed in the lighter poly(ethylene glycol)-rich phase. The interfacial tensions, gamma, between the phases were determined with the pendant drop method, and a linear relationship was found between gamma-1/2 and the cosine of the angle the droplets made with the cell layers (Good-Girifalco plot). We were thus able to determine the limiting or critical interfacial tension, gamma c, for spreading on the cell layers. The value of gamma c is a measure of the interfacial energy of the cell/bathing medium interface. Values of gamma c obtained by this method include the following: 0.65 and 0.84 microN . m-1 for human erythrocytes and neutrophils, respectively; 0.93 microN . m-1 for porcine pulmonary macrophages; 0.75--3.60 microM . m-1 for various transformed murine lymphoid cell lines, and 2.53 microN . m-1 for Balb/c murine spleen lymphocytes. Exposure to various agents has differing effects on gamma c. Concanavalin A reduces gamma c, and bacterial lipopolysaccharide increases gamma c of murine spleen lymphocytes. The calcium ionophore, A23187, increases gamma c of both porcine pulmonary macrophages and murine spleen lymphocytes. This new method provides a quantitative approach to the cell surface energy and hydrophobicity which are thought to play an important role in membrane-mediated phenomena and in cell adhesion.
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PMID:Determination of cell/medium interfacial tensions from contact angles in aqueous polymer systems. 616 85


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