Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P43026 (lipopolysaccharide)
 62,215 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Actinobacillus actinomycetemcomitans is a gram-negative capnophilic coccobacillus that has been implicated in the etiology of certain forms of early-onset periodontitis as well as non-oral infections, mostly bacterial endocarditis. Five distinct serotypes of A. actinomycetemcomitans have been described. Although the O-polysaccharide (O-PS) of lipopolysaccharide (LPS) has been shown to define the serologic specificity for this species, only the structure of the O-PS of serotype b has been characterized. The focus of the current study was to define the structures of the O-PS of A. actinomycetemcomitans serotypes a, c, d and e. Structure determination was accomplished through the use of methylation, periodate oxidation, and one-dimensional and two-dimensional NMR methods. The O-PS of A. actinomycetemcomitans (OMZ-542) serotype d had [alpha]D +15 degrees and was composed of D-glucose, D-mannose and L-rhamnose (L-Rha) in a molar ratio of 1:2:1. Methylation, periodate oxidation, and two-dimensional 1H-NMR and 13C-NMR studies showed that the antigenic O-PS was a high-molecular-mass polymer composed of repeating tetrasaccharide units with the structure: [formula: see text] The O-PS of the LPS produced by A. actinomycetemcomitans (ATCC 29523) serotype a had [alpha]D +150 degrees and was found to contain 6-deoxy-D-talose (6dTalp) and O-acetyl (2:1) and was a high-molecular-mass polymer composed of O-acetyl-substituted repeating disaccharide units with the structure: [formula: see text] The O-PS of the LPS of A. actinomycetemcomitans (SUNY 67) serotype c had [alpha]D -170 degrees and was composed of 6-deoxy-L-talose and O-acetyl (2:1). Structural analysis showed that the O-PS was a high-molecular-mass polymer of repeating disaccharide units with the structure: [formula: see text] The O-PS of the LPS of A. actinomycetemcomitans (OMZ 534) serotype e had [alpha]D +57 degrees and was composed of 2-acetamido-2-deoxy-D-glucose and L-rhamnose (1:1) and by chemical and NMR analysis was found to be a polymer of repeating disaccharide units with the structure: -->4)-alpha-D-GlcpNAc-(1-->3)-alpha-L-Rhap-(1-->.
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PMID:Structures of the antigenic O-polysaccharides of lipopolysaccharides produced by Actinobacillus actinomycetemcomitans serotypes a, c, d and e. 902 97

Periodontal disease is a significant cause of alveolar bone resorption resulting ultimately in the loss of teeth. Inflammation of the periodontal tissues is initiated by bacteria of the oral micro-flora. Invading micro-organisms stimulate both protective and destructive inflammatory-immune responses involving cytokine release syndrome, chemokines, arachidonic acid metabolites, reactive oxygen and nitrogen intermediates, and matrix melloproteinases. The local infection may affect general health in two ways. First, transient bacteremia from the oral focus may result in metastatic infection in remote organs of susceptible hosts, such as bacterial endocarditis in patients with congenital or acquired heart diseases. Second, lipopolysaccharide and inflammatory mediators are not only involved in local tissue destruction but have the potential to modulate the course of cardiovascular, chronic obstructive lung and autoimmune diseases, diabetes mellitus and preterm birth. Epidemiologic observations, awaiting further verification by controlled prospective trials, underline the impact of oral health on general well-doing.
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PMID:[Periodontal disease and general health--literature review]. 1198 Apr 26

The pathogenesis of very severe thrombocytopenia in bacterial endocarditis is uncertain. We report a 50-year-old male with platelet counts < 10 x 10(9)/l and fragmentation hemolysis complicating Staphylococcus epidermidis pacemaker endocarditis with a giant vegetation. Antibiotics, corticosteroids, high-dose intravenous gammaglobulin, and plasmapheresis (for initially-suspected thrombotic thrombocytopenic purpura) failed to produce significant platelet count increase. However, therapeutic-dose heparin anticoagulation was associated with a platelet count increase from <10 to approximately 40 x 10(9)/l, with parallel reduction in thrombin-antithrombin complexes (from 8.9 to 3.5 microg/l), facilitating surgical intervention. The thrombocytopenia promptly resolved following surgical removal of the vegetation. Culture supernatant from S. epidermidis isolated from the patient's blood induced monocytes to express procoagulant activity (assessed by factor Xa generation) equivalent to lipopolysaccharide (1 microg/ml), with half-maximal activation seen with culture supernatant diluted to 1:12,800. These data are consistent with previous animal models of endocarditis demonstrating staphylococci-induced procoagulant changes in monocytes. This case demonstrates that heparin anticoagulation can be therapeutic in infective endocarditis-associated severe thrombocytopenia in a non-bleeding patient, and that such therapy may ameliorate the platelet count enough to permit surgical intervention.
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PMID:Very severe thrombocytopenia and fragmentation hemolysis mimicking thrombotic thrombocytopenic purpura associated with a giant intracardiac vegetation infected with Staphylococcus epidermidis: role of monocyte procoagulant activity induced by bacterial supernatant. 1716 Sep 89