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

A soluble hydrophilic lipopolysaccharide, termed lipopolysaccharide II, isolated from Proteus mirabilis, strain D52 contained N-acetylglucosamine, glucose, galactose, ribitol phosphate and ethanolamine phosphate as constituents of the O-specific polysaccharide. Periodate oxidation studies were carried out on the polymer before and after dephosphorylation with hydrofluoric acid and on oligosaccharides derived from the polymer by partial acid hydrolysis. The results obtained indicate that the polysaccharide chain consists of the chemical repeating unit Gal-1,3(4)-GlcNAc-1,3-Glc-1,3-GlcNAc-, where GlcNAc stands for N-acetylglucosamine. Whereas the galactose residue is substituted at C-3 by ribitol phosphate, the glucose is substituted by ethanolamine phosphate at C-6.
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PMID:The ribitol-phosphate-containing lipopolysaccharide from Proteus mirabilis, strain D52. Investigations on the structure of O-specific chains. 32 5

A procedure is described for the selection of conditional 3-deoxy-D-manno-octulosonic-acid--Lipid A mutants which depends on temperature sensitivity for both synthesis of complete lipopolysaccharide and for growth. Using this procedure new types of mutants were isolated which cease growth and accumulate lipid A precursors following a shift to nonpermissive temperatures. All precursor molecules differ in their charge as judged by DEAE-cellulose chromatography. While they all contain glucosamine, phosphate and 3-hydroxymyristic acid, they lack detectable 3-deoxy-D-manno-octulosonic acid (dOclA) as well as the nonhydroxylated fatty acids of the complete lipid A structure. Three mutants proved to be conditionally defective in dOclA metabolism, whereas one seems to be blocked at a relatively early step in lipid A synthesis. The phenotypes of all these mutants appear to be due to single mutations by reversion analysis and by characterization of the temperature-resistant revertants. Studies of these mutants may shed light on the essential role of the complete dOclA--lipid A part of lipopolysaccharides in membrane function.
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PMID:Isolation of mutants conditionally blocked in the biosynthesis of the 3-deoxy-D-manno-octulosonic-acid--lipid-A part of lipopolysaccharides derived from Salmonella typhimurium. 32 82

Two fatty acyl amidases have been partially purified from the slime mold, Dictyostelium discoideum. Their action on lipopolysaccharide derivatives, especially Compound I, has been studied. Amidase I removes specifically the beta-hydroxymyristyl group, which is present on the amino group adjacent to the C-1 phosphate. The product, Compound V, is then a substrate for Amidase II, which removes the remaining beta-hydroxymyristyl group from the amino group in the distal glucosamine ring to give Compound VI. Compound I itself is resistant to Amidase II. Thus, the two enzymes show a high degree of structural specificity. The structure of lipopolysaccharide from the E. coli K-12 mutant is concluded in the light of studies reported in this and the accompanying papers, and this structure is discussed in relation to other bacterial lipopolysaccharides.
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PMID:The structure of lipopolysaccharide from an Escherichia coli heptose-less mutant. III. Two fatty acyl amidases from Dictyostelium discoideum and their action on lipopolysaccharide derivatives. 37 23

Two genetically distinct classes of novobiocin-supersensitive mutants were isolated from Escherichia coli K-12. One class, given the phenotypic name NbsA, lies at 10 min on the E. coli chromosome. The order of the genes in this region, based on transductional analyses, is proC NbsA plsA purE. The second, NbsB, lies at 80 min. The order of the genes in this region, based on transduction analyses, is xyl cysE NbsB pyrE. Both classes of mutants show increased sensitivity to hydrophobic drugs but are different: NbsA cells tend to be more sensitive to cationic agents, whereas NbsB cells show the opposite tendency. The sole detectable biochemical alteration in NbsA strain is greater than 90% reduction in the phosphate content of the lipid A region of the lipopolysaccharide. The NbsB mutation results in lipopolysaccharide that contains primarily the stereoisomer D-glycero-D-mannoheptose, rather than L-glycero-D-mannoheptose, and which contains very little of the distal sugars. Since NbsA strains have apparently normal outer membrane proteins and total cellular phospholipids, changes solely in lipopolysaccharide can increase permeability to certain hydrophobic antibiotics. Complementation studies indicate that the NbsA marker is probably allelic with acrA. In addition, the NbsB marker is genetically and phenotypically similar to the rfaD locus of Salmonella typhimurium. For this reason, the phenotypic designations NbsA and NbsB have been changed to the genotypic designations acrA and rfaD, respectively.
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PMID:Two mutations which affect the barrier function of the Escherichia coli K-12 outer membrane. 38 99

Freeze fracturing electron microscopy of Escherichia coli K12 cells showed that the outer fracture face of the outer membrane is densily occupied with particles. On the inner fracture face of the outer membrane, pits are visible, which are probably complementary to the particles at opposite fracture face. This observation suggests that the particles are micelle-like. In some mutants which lack one or more major outer membrane proteins the density of particles is reduced. The loss of protein d appeared to a prerequisite for this phenomenon. However, mutants which lack all glucose and heptose-bound phosphate in their lipopolysaccharide also have a reduction in particle density whereas, the amount of protein d is normal. Moreover, loss of lipopolysaccharide by EDTA treatment also caused a reduction in the density of particles. From these results it is hypothesized that the particles consist of lipopolysaccharide aggregates stabilized by divalent cations and probably complexed with protein and/or phospholipid.
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PMID:Architecture of the outer membrane of Escherichia coli K12. II. Freeze fracture morphology of wild type and mutant strains. 40 48

Exponentially grown cells of Escherichia coli K-12 heated at 48 degrees C in potassium phosphate buffer at pH 7.0 were structrually injured before death. During heating for 60 min about 20% of the cellular lipopolysaccharide (LPS) was released from the outer membrane into the heating medium. Removal of 30% of the cellular LPS, by washing the cells in buffer containing ethylenediaminetetraacetic acid (EDTA), caused no significant increase in the rate of death and structural injury produced by heating. The addition of EDTA to the heating medium produced only a slight increase in the rate of thermal death but a large increase in the rate of structural injury. By a combination of heating at 48 degrees C and washing with EDTA, a maximum of 50% of the LPS was released from cells. These results taken together suggest that structural injury and loss of LPS are not the direct causes of death. The addition of 5 m M Mg2+ to the heating medium protected the cells from death and structural injury caused by heating at 48 degrees C.
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PMID:Outer-membrane damage in sublethally heated Escherichia coli K-12. 40 6

Studies in our laboratory with both the monkey and the rat showed that, after three hours of endotoxemia, there was a significant decrease in the number of circulating platelets, total hemolytic complement (CH 50 units), and blood serotonin (5-HT) levels. Administration of dexamethasone sodium phosphate in the clinical dose range at the time of endotoxin challenge significantly attenuated the decrease in blood 5-HT levels when compared to the untreated groups in both the monkey and the rat experiments. In the monkey, CH 50 units remained at a higher level when dexamethasone was administered; however, the difference between the treated and untreated groups was not statistically significant. The number of circulating white blood cells and platelets did not appear to be significantly altered by corticosteroid treatment. It is suggested that glucocorticoids may interfere with lipopolysaccharide-induced alterations in complement components or factors regulating hemostasis that influence platelet 5-HT release.
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PMID:Endotoxin-challenged monkeys and rats. 41 99

A serologically active, acidic arabinomannan has been isolated from Mycobacterium smegmatis. The polysaccharide contains approximately 56 arabinosyl and 11 mannosyl residues, and 2 phosphate, 6 monoesterified succinate, and 4 ether-linked lactate groups. After saponification to remove succinyl groups, the polysaccharide can be separated into phosphorylated (55%) and nonphosphorylated (45%) forms, the former containing a little more arabinose and a little less mannose than the latter. The structures of these polysaccharides were investigated by 1H- and 13C-n.m.r. spectroscopy and methylation analysis, before and after selective cleavage of furanosyl linkages. The phosphorylated and nonphosphorylated forms of the polysaccharide were found to have similar, if not identical, structures. The main structural feature of the polysaccharides is the presence of chains of contiguous arabinofuranosyl residues linked alpha-(1 leads to 5). These chains are attached at 0-4 of arabinopyranosyl residues that are present in a core region of the polysaccharide that also contains mannopyranosyl residues. Immunochemical studies demonstrated that the polysaccharide is an effective, precipitating antigen with antisera from rabbits immunized with cell walls or heat-killed cells of M. smegmatis. The polysaccharide is, however, more effective as a precipitating antigen after removal of the succinate groups, and completely ineffective after removal of arabinofuranosyl residues. The polysaccharide therefore contains an important antigen in common with the arabinogalactan lipopolysaccharide of the cell wall of the bacterium, i.e., chains of contiguous alpha-(1 leads to 5)-linked arabinofuranosyl residues.
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PMID:Structural and immunochemical characterization of the acidic arabinomannan of Mycobacterium smegmatis. 57 62

Untreated and partially deacylated lipopolysaccharides from various P- and P+ strains of Salmonella were studied with 31P nuclear magnetic resonance spectroscopy and by conventional analytical methods. The spectral signals were assigned to various phosphate groups in the lipid A moiety and in the oligosaccharide part. A signal at +2.3 ppm could be assigned to a phosphodiester linkage formed between 4-amino-4-deoxyl-L-arabinose linked via the glycosidic hydroxyl group to the 4'-phosphate group of the glucosamine disaccharide in the lipid A moiety. A strong pyrophosphate signal at +11 ppm in P- strains was identified as a pyrophosphoryl ethanolamine group at the glycosidic end of this glucosamine disaccharide unit. No evidence was found for phosphodiester or pyrophosphodiester bonds crosslinking lipopolysaccharide 'subunits'. A revised version of the lipid A structure of Salmonella is presented. By a combination of 31P nuclear magnetic resonance spectroscopy data and conventional analytical methods the extent to which the lipopolysaccharides are substituted by various phosphate groups on the lipid A and the oligosaccharide moiety could be estimated. It was thus shown that substantial heterogeneity, leading to several molecular species of lipopolysaccharides is caused by addition or omission of certain groups. Since changes in substitution were found to be dependent on the growth conditions, it is thought possible that the overall negative surface charge of Salmonella can be modified by addition or omission of neutralising amino groups from ethanolamine and/or 4-amino-4-deoxy-L-arabinose, and can thus be adapted to the environment.
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PMID:A 31P-nuclear-magnetic-resonance study of the phosphate groups in lipopolysaccharide and lipid A from Salmonella. 59 Feb 67

Lipopolysaccharide O antigens (endotoxins) and other bacterial antigens readily attach to erythrocytes in vitro. This attachment is prevented by certain mammalian and avian sera. In this study, the inhibitory capacity of sera from lower animals was compared with that of higher animals for a total of 30 species. Antigens and the corresponding antisera included both crude O antigens and purified lipopolysaccharide preparations, the common enterobacterial antigen from Escherichia coli O14, the Vi antigen from Citrobacter ballerup, the polyribose-phosphate antigen from Haemophilus influenzae type b, and the crude teichoic acid antigen from Staphylococcus aureus. Antigen and serum mixtures were incubated at 37 degrees C for 30 min and used for erythrocyte modification; failure of hemagglutination by homologous bacterial antiserum provided evidence of inhibitory capacity. Sera from the classes Mammalia and Aves were very strong inhibitors; those of Reptilia and Osteichthyes were moderate in activity, displaying variation within the classes; those of Amphibia and Chondrichthyes were minimal inhibitors; and those of Merostomata, Crustacea, and Lamellibranchiata displayed questionable or no inhibitory capacity. Inhibitory sera were active with all antigens tested. The findings suggest evolution of inhibitory factors consistent with the theory of two diverging lines of animal phylogeny based on embryological criteria and closely parallel the observations of an endotoxin-altering capacity in vertebrate sera that is not found in invertebrate sera or hemolymph.
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PMID:Effect of serum from various animal species on erythrocyte attachment of endotoxins and other bacterial antigens. 59 Oct 59


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