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

Peripheral blood mononuclear cells (MNC) from 27 children with a febrile convulsion were tested for production of interleukin-1 (IL-1) in culture. MNC stimulated with lipopolysaccharide (LPS) showed a significantly increased production of IL-1 when compared to MNC from children without convulsions but with bacterial infections (p less than 0.001), viral infections (p less than 0.005) or no infection (p less than 0.005). Children who had experienced a febrile convulsion were retested several months later; this time the IL-1 production from LPS-stimulated MNC was not different from controls. These results demonstrate that MNC at the time of febrile convulsions have increased sensitivity to LPS and possibly to other IL-1 inducers; the resulting enhanced IL-1 response from sensitized MNC may have a role in the pathogenesis of febrile convulsions.
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PMID:Increased interleukin-1 (IL-1) production from LPS-stimulated peripheral blood monocytes in children with febrile convulsions. 223 77

In group C1 salmonellae, rfe and rff genes linked to the ilv locus specify the synthesis of a glycolipid called the enterobacterial common antigen. In contrast, in group B salmonellae the synthesis requires in addition some of the genes in the rfb cluster, the main genetic determinant of the O side chains of lipopolysaccharide. In an effort to define the biochemical functions of these rfb genes, we looked in Salmonella typhimurium LT2 (group B) for rfb mutants in which the synthesis of both enterobacterial common antigen and the O side chains would be blocked in a manner suppressible by the wild-type rfe cluster of S. montevideo, of group C1. We found one mutant with these characteristics. This rfb mutation affected the activity of dTDPglucose pyrophosphorylase (glucose-1-phosphate thymidylyltransferase, EC 2.7.7.24). Whereas the rfe cluster of S. montevideo contained a gene producing this enzyme activity, there was no evidence for the presence of such a gene in the rfe cluster of group B strains. These results also showed that the synthesis of dTDP-glucose is necessary for the biosynthesis of enterobacterial common antigen; this conclusion fits with the recent demonstration of 4-acetamido-4,6-dideoxy-D-galactose as a component of enterobacterial common antigen (Lugowski et al., Carbohydr. Res. 118:173-181, 1983), because the biosynthesis of the donor of this sugar, dTDP-4-acetamido-4,6-dideoxy-D-galactose, requires dTDPglucose pyrophosphorylase.
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PMID:Biosynthesis of enterobacterial common antigen requires dTDPglucose pyrophosphorylase determined by a Salmonella typhimurium rfb gene and a Salmonella montevideo rfe gene. 243 Sep 41

The gram-negative organism causing abortion in dogs was examined in parallel with cultures representative of the Brucella species and with Bordetella bronchiseptica. The organism fits into the genus Brucella and most closely resembles B. suis on the basis of its growth characteristics. It is of rough colonial morphology and is agglutinated by antisera prepared against rough Brucella. In mouse toxicity tests, no endotoxic activity could be demonstrated. In contrast to most Brucella cultures, it does not utilize erythritol. Electron microscopy showed a cell wall structure similar to that of other gram-negative organisms. The question of whether the organism should be designated Brucella canis, as proposed by Carmichael and Bruner, or Brucella suis biotype 5 is discussed. The authors favor the designation Brucella canis because the organism lacks the lipopolysaccharide antigen associated with the smooth agglutinogen and endotoxin, and it does not utilize erythritol.
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PMID:Taxonomic position in the genus Brucella of the causative agent of canine abortion. 568 22

We report the identification and sequence from Escherichia coli and Salmonella enterica strains of the cld gene, encoding the chain-length determinant (CLD) which confers a modal distribution of chain length on the O-antigen component of lipopolysaccharide (LPS). The distribution of chain lengths in the absence of this gene fits a model in which as the chain is extended there is a constant probability of 0.165 of transfer of growing chain to LPS core, with termination of chain extension. The data for E. coli O111 fit a model in which the CLD reduces this probability for short chains and increases it to 0.4 for longer chains, leading to a reduced number of short chain molecules but an increase in numbers of longer molecules and transfer of essentially all molecules by chain length 21. We put forward a model for O-antigen polymerase which resembles the ribosome and fatty acid synthetase in having two sites, with the growing chain being transferred from a D site onto the new unit at the R site to extend the chain and then back to the D site to repeat the process. It is proposed that the CLD protein and polymerase form a complex which has two states: 'E' facilitating extension and 'T' facilitating transfer to core. The complex is postulated to enter the E state as O-antigen polymerization starts, and to shift to the T state after a predetermined time, the CLD acting as a molecular clock. The CLD is not O-antigen or species-specific but the modal value does depend on the source of the cld gene.
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PMID:Repeat unit polysaccharides of bacteria: a model for polymerization resembling that of ribosomes and fatty acid synthetase, with a novel mechanism for determining chain length. 768 79

A Drosophila UDP-glucose:glycoprotein glucosyltransferase was isolated, cloned and characterized. Its 1548 amino acid sequence begins with a signal peptide, lacks any putative transmembrane domains and terminates in a potential endoplasmic reticulum retrieval signal, HGEL. The soluble, 170 kDa glycoprotein occurs throughout Drosophila embryos, in microsomes of highly secretory Drosophila Kc cells and in small amounts in cell culture media. The isolated enzyme transfers [14C]glucose from UDP-[14C]Glc to several purified extracellular matrix glycoproteins (laminin, peroxidasin and glutactin) made by these cells, and to bovine thyroglobulin. These proteins must be denatured to accept glucose, which is bound at endoglycosidase H-sensitive sites. The unusual ability to discriminate between malfolded and native glycoproteins is shared by the rat liver homologue, previously described by A.J. Parodi and coworkers. The amino acid sequence presented differs from most glycosyltransferases. There is weak, though significant, similarity with a few bacterial lipopolysaccharide glycotransferases and a yeast protein Kre5p. In contrast, the 56-68% amino acid identities with partial sequences from genome projects of Caenorhabditis elegans, rice and Arabidopsis suggest widespread homologues of the enzyme. This glucosyltransferase fits previously proposed hypotheses for an endoplasmic reticular sensor of the state of folding of newly made glycoproteins.
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PMID:Drosophila UDP-glucose:glycoprotein glucosyltransferase: sequence and characterization of an enzyme that distinguishes between denatured and native proteins. 772 8

An approach for studying neurotoxicity of bacterial products is presented. Pentylenetetrazol, a convulsant drug, was injected into mice, and increased sensitivity to pentylenetetrazol was used as an indicator of neurotoxicity. The preinjection of sonicates of Shigella dysenteriae 60R or Escherichia coli H30 (producing Shiga toxin or Shiga-like toxin I, respectively) enhanced the response of mice to pentylenetetrazol within 6 h. This was indicated by a higher mean convulsion score, increased number of mice responding with convulsions, and induction of seizures in animals pretreated with a subepileptic dose of pentylenetetrazol. Preinjection of purified Shiga toxin significantly changed the response to pentylenetetrazol only when coadministered with bacterial lipopolysaccharide (LPS); mean convulsion scores were 1.6 and 0.9 for the Shiga toxin-LPS group and controls, respectively. LPS alone did not affect sensitivity to pentylenetetrazol. These results suggest that Shiga toxin and LPS together induce neurologic disorders early in the course of infection.
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PMID:An animal model for the study of neurotoxicity of bacterial products and application of the model to demonstrate that Shiga toxin and lipopolysaccharide cooperate in inducing neurologic disorders. 775

Platelets contain a large amount of 5-hydroxytryptamine (5HT, serotonin). Intravenous injection into BALB/c mice of a Boivin's preparation of lipopolysaccharide (LPS) from Escherichia coli induced rapid 5HT accumulation in the lung (within 5 min) and slow 5HT accumulation in the liver (2 to 5 h later). The rapid response required high doses of LPS (more than 0.1 mg/kg). On the basis of 5HT measurements, 70% or more of the platelets which disappeared from the blood appeared to have accumulated rapidly in the lung, and a large number of platelets were found there by electron microscopy. A shock, which was manifested by crawling, convulsion, or prostration, followed shortly after the rapid accumulation of 5HT in the lung. On the other hand, the slow accumulation of 5HT in the liver could be induced by much lower doses of LPS (1 microg/kg or less), even when given by intraperitoneal injection. This 5HT accumulation appears to be a reflection of platelet accumulation in the liver (Y. Endo and M. Nakamura, Br. J. Pharmacol. 105:613-619, 1992). The combination of a low dose of LPS with D-galactosamine amplified the hepatic accumulation of 5HT, and the mice developed a severe hepatic congestion resulting in death. The rapid response was not induced at all in C3H/HeN mice. These results and comparison with other LPS preparations indicate that some component(s) of LPS from E. coli induces a biphasic, organ-specific and strain-specific accumulation of platelets, and it is proposed that this effect is involved in the development of shock.
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PMID:Biphasic, organ-specific, and strain-specific accumulation of platelets induced in mice by a lipopolysaccharide from Escherichia coli and its possible involvement in shock. 894 79

Monoclonal, murine IgG1s S-20-4, A-20-6, and IgA 2D6, directed against Vibrio cholerae O:1 Ogawa-lipopolysaccharide exhibited the same fine specificities and similar affinities for the synthetic methyl alpha-glycosides of the (oligo)saccharide fragments mimicking the Ogawa O-polysaccharide (O-PS). They did not react with the corresponding synthetic fragments of Inaba O-PS. IgG1s S-20-4 and A-20-6 have absolute affinity constants for synthetic Ogawa mono- to hexasaccharides of from approximately 10(5) to approximately 10(6) M-1. For IgG1s S-20-4, A-20-6, and IgA 2D6, the nonreducing terminal residue of Ogawa O-PS is the dominant determinant, accounting for approximately 90% of the maximal binding energy shown by these antibodies. Binding studies of derivatives of the Ogawa monosaccharide and IgGs S-20-4 and A-20-6 revealed that the C-2 O-methyl group fits into a somewhat flexible antibody cavity and that hydrogen bonds involving the oxygen and, respectively, the OH at the 2- and 3-position of the sugar moiety as well as the 2'-position in the amide side chain are required. Monoclonal IgA ZAC-3 and IgG3 I-24-2 are specific for V. cholerae O:1 serotypes Ogawa/Inaba-LPS.1 The former did not show binding with members of either series of the synthetic ligands related to the O-antigens of the Ogawa or Inaba serotypes, in agreement with its reported specificity for the lipid/core region (1). Inhibition studies revealed that the binding of purified IgG3 I-24-2 to Ogawa-LPS might be mediated by a region in the junction of the OPS to the lipid-core region of the LPS. cDNA cloning and analysis of the anti-Ogawa antibodies S-20-4, A-20-6, and 2D6 revealed a very high degree of homology among the heavy chains. Among the light chains, no such homology between S-20-4 and A-20-6 on the one hand, and 2D6 on the other hand, exists. For the anti-Inaba/Ogawa antibodies I-24-2 and ZAC-3, their heavy chains are completely different, with some homology among the light chains.
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PMID:On the antigenic determinants of the lipopolysaccharides of Vibrio cholerae O:1, serotypes Ogawa and Inaba. 944 85

Defects involving cellular expression of activation molecules, cell mediated immune response and natural killer (NK) activity are commonly observed in the elderly. Herein, data are reported on the evaluation of IL-12 production by old subjects. IL-12 is, actually, considered the key molecule for the induction of a T helper 1 (Th1) -type and NK response. IL-12 production from old subjects peripheral blood mononuclear cells (PBMNC) was evaluated using T-independent (bacterial lipopolysaccharide, LPS) or -dependent (phytoemagglutinin, PHA; immobilized anti-CD3 monoclonal antibodies, anti-CD3) mitogens. The IL-12 production after LPS stimulation was not reduced in cultures from old subjects when compared to that from young ones. On the contrary, IL-12 production by PHA or anti-CD3 stimulated PBMNC from old subjects was decreased. Furthermore, we have demonstrated a reduced CD40 and CD40 ligand (CD40L) expression on PBMNC from old subjects. This finding fits very well with the reduced cytokine production observed in the T-dependent stimulation systems, being the CD40-CD40L interaction mandatory for an efficient IL-12 production. All together, these results seem to suggest that defects in cell expression of activation molecules can affect the IL-12 secretion and in consequence other Th1-type cytokines.
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PMID:Interleukin-12 release by mitogen-stimulated mononuclear cells in the elderly. 972 Jun 53

A major controversy in human epilepsy is whether severe seizures in infants or young children cause brain damage and subsequent epilepsy. Kainic acid (KA) produces severe seizures in infant rats, but hippocampal neuronal death and mossy fibre sprouting have not been previously demonstrated. There are similarities between lipopolysaccharide (LPS) pretreatment and KA-induced seizures in rats and the febrile convulsion of young children, in that both processes are associated with an immune stimulus and seizures. Infant rats, co-treated with LPS and KA, showed hippocampal neuronal death and mossy fibre sprouting. Taken together, our results suggest that severe febrile convulsion of young children may cause hippocampal damage and synaptic reorganization.
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PMID:Kainic acid-induced seizures cause neuronal death in infant rats pretreated with lipopolysaccharide. 1071 4


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