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)

It is well established that plasmids are involved in the expression of lipopolysaccharide in certain species of Shigella. In Shigella sonnei, both the biosynthesis of oligosaccharide side chains (O antigen), and cell invasiveness are controlled exclusively by a 120 megadalton (MDa) plasmid. In Shigella dysenteriae 1, a 10 kilobase (kb) plasmid is required for O-antigen production. Shigella dysenteriae 1 strains devoid of this plasmid lose the ability to synthesize O antigen. Interestingly, this 10-kb plasmid is not stably maintained in Escherichia coli K-12 strains, where it is lost spontaneously at a high frequency. Our genetic analyses of Shigella dysenteriae 1 strain IDBM11 and its derivatives indicate that the stability of this plasmid is associated with the histidine region of the chromosome which is unique to Shigella dysenteriae. Furthermore, the 10-kb plasmid is stably maintained in wild-type IDBM11 with an intact histidine locus. However, this plasmid is not stable in IDBM11 derivatives (e.g., IDBM11-1 and IDBM11-2), in which the his locus has been substituted with the histidine region of an E. coli K-12 chromosome. The S. dysenteriae IDBM11 strain, and its derivatives (lacking a 10-kb plasmid), displayed an invasive property as demonstrated by their internalization by HeLa cells in an in vitro assay. Thus the 10-kb plasmid of Shigella dysenteriae 1 is required for O-antigen synthesis but not for cell invasion.
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PMID:The stability of O-antigen plasmid is determined by a chromosomal region of Shigella dysenteriae 1. 245 51

Recent studies have shown that determinants for the production of O antigen lipopolysaccharide in Shigella dysenteriae 1 are distributed over two distinct genetic elements, the chromosome and a 9 kb plasmid designated pHW400. In this communication, we describe the cloning of all determinants necessary for S. dysenteriae 1 O antigen production in E. coli K-12 and their combination in a single plasmid. An RP4::miniMu R-prime plasmid, R-prime 40, containing the his-rfb (histidine biosynthesis-lipopolysaccharide biosynthesis) gene region of the Shigella dysenteriae 1 chromosome was generated. E. coli K-12 bacteria containing R-prime 40 and pSS8, a transposon Tn5-tagged derivative of pHW400, produced lipopolysaccharide indistinguishable from that of S. dysenteriae 1. Small DNA fragments containing the rfb gene cluster and the rfp gene were subcloned from R-prime 40 and pSS8 and subsequently combined in vector pACYC184 to produce pSS37. This latter plasmid when introduced by transformation into E. coli K-12 provoked the formation of S. dysenteriae 1 O-specific lipopolysaccharide, a feature that suggests it may be useful in the construction of LPS-based live vaccines against the Shiga bacillus.
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PMID:Cloning of the rfb gene region of Shigella dysenteriae 1 and construction of an rfb-rfp gene cassette for the development of lipopolysaccharide-based live anti-dysentery vaccines. 246 31

Production of the somatic antigen, O-specific polysaccharide of Shigella dysenteriae 1 is determined by the chromosomal rfb gene cluster and the rfp gene located on the 9 kb plasmid pHW400 carried by this organism. When transferred to Escherichia coli K-12, which produces lipopolysaccharide consisting only of core oligosaccharide linked to lipid A, rfp gene-containing plasmids caused modification of the core oligosaccharide leading to the appearance of core molecules with new electrophoretic mobilities. Chemical analysis of the modified core has shown that it is substituted with a galactose residue which is the first sugar of the O-polysaccharide repeat unit.
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PMID:Genetic and biochemical analysis of Shigella dysenteriae 1 O antigen polysaccharide biosynthesis in Escherichia coli K-12: 9 kb plasmid of S. dysenteriae 1 determines addition of a galactose residue to the lipopolysaccharide core. 246 32

The interferon (IFN)-inducing activity of detoxified lipopolysaccharide (LPS) was tested in rabbits treated with LPS preparation derived from Escherichia coli, Salmonella typhi, Salmonella enteritidis and Shigella dysenteriae serovar 1. Of the detoxification procedures used, alkaline hydrolysis, hydroxylaminolysis, formalization, treatment with sodium deoxycholate and the radiodetoxification (fast or slow) methods had no appreciable effects on the IFN-inducing potential of LPS. In contrast, acetylation or prolonged alkaline hydrolysis of LPS resulted in up to a 9-fold reduction of IFN-induction capacity and effects of Cu++ or Fe++ cations bound to LPS were clearly inhibitory (Fe more than Cu).
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PMID:Effect of detoxification processes on the interferon-inducing activity of bacterial endotoxins. 248 74

Outbreaks of Shigella dysenteriae I occurred in northeastern Thailand in the fall of 1986 and again in the spring and fall of 1987 for the first time in over 20 years. The epidemic strain of S. dysenteriae I was resistant to tetracycline, streptomycin, chloramphenicol, and trimethoprim-sulfamethoxazole, but susceptible to ampicillin. Trimethoprim resistance was chromosomally encoded by type I dihydrofolate reductase. In Ubon Province, where 10,000 cases of dysentery were reported, there were 3-5 cases of dysentery per 1,000 residents during the peak months, with 2-5 hospitalizations per 100 cases of reported dysentery. There were 2 deaths among 101 hospitalized, culture-confirmed cases. The overall case-fatality rate among reported cases of dysentery in this province was 0.9%. In contrast to S. flexneri infections, which occurred predominantly among children less than 5 years old, S. dysenteriae I infections occurred in all age groups. The large number of susceptibles appeared to be important in allowing rapid spread of S. dysenteriae I. In 1 village, 46% of 434 villagers reported dysentery; S. dysenteriae I was isolated from 24 out of 81 (30%) individuals cultured. Based on the prevalence of IgG antibody to S. dysenteriae I lipopolysaccharide, it was estimated that 76% of the villagers had been infected.
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PMID:Introduction and spread of multi-resistant Shigella dysenteriae I in Thailand. 264 59

The role of plasmids in the virulence of Shigella dysenteriae 1 W30864, which contains at least five species, was investigated. By means of a standard plasmid-curing procedure, that is, bacterial cultivation at an elevated temperature, five virulence-deficient derivatives were obtained. One of these lacked a small, 6-megadalton plasmid, designated pHW400, exhibited reduced invasiveness for HeLa cells, and failed to produce the somatic antigen. Transposon tagging of the pHW400 plasmid to produce pHW401 and the transfer of this derivative into a variant of strain W30864 lacking pHW400 confirmed the conclusion that the pHW400 plasmid encodes one or more functions involved in O antigen (lipopolysaccharide) biosynthesis and bacterial virulence. A plasmid of similar size was detected in all of the three other strains of S. dysenteriae 1 examined.
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PMID:A small plasmid in Shigella dysenteriae 1 specifies one or more functions essential for O antigen production and bacterial virulence. 636 Sep 5

A 6-megadalton plasmid, pHW400, of Shigella dysenteriae 1 strain W30864 was previously found to specify one or more functions for O-antigen production and bacterial virulence (H. Watanabe and K. N. Timmis, Infect. Immun. 43:391-396, 1984). The region of pHW401, a Tn801-tagged derivative of pHW400, responsible for O-antigen production has been localized by gene cloning and Tn5 transposon mutagenesis. Analysis of lipopolysaccharide isolated from S. dysenteriae 1 bacteria carrying mutant plasmids revealed that the determinant for O-antigen synthesis, designated rfp, codes for a function involved in the formation of the O-polysaccharide side chain structure of lipopolysaccharide. Analysis of radioactively labeled proteins synthesized in minicells of Escherichia coli carrying mutant plasmids identified the product of the rfp gene as a 41,000-dalton protein. Southern hybridization with a DNA fragment carrying the rfp gene demonstrated that this determinant is present on 6-megadalton plasmids in other isolates of S. dysenteriae 1 but is not present at all in a variety of other Shigella, E. coli, and Salmonella typhimurium strains that were tested.
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PMID:Small virulence plasmid of Shigella dysenteriae 1 strain W30864 encodes a 41,000-dalton protein involved in formation of specific lipopolysaccharide side chains of serotype 1 isolates. 638 48

An enzyme-linked immunosorbent assay (ELISA) for determining the class-specific humoral antibody response to the lipopolysaccharide antigen from Shigella dysenteriae serotype 1 bacteria has been tested. Two or more serum samples from each of 60 persons infected with this organism during a dysentery outbreak in a boarding school for young men near Haiphong, Viet Nam, and single serum samples from 39 healthy Vietnamese and from 20 healthy Swedes were included in the study. Comparison of the titres in the sera from the patients and the Vietnamese controls showed that the patients had significantly elevated IgA titres in sera collected 10, 30 and 45 days after onset of infection, and significantly elevated IgG titres in sera collected 30, 45 and 180 days after the onset. The titres in the patients' sera, compared with those in the Swedish controls, were significantly elevated for IgA and IgM as well as IgG in the samples collected after 10, 30, 45 and 180 days. The use of rabbit antisera, specific for enteropathogenic bacteria, and absorption experiments with human sera indicated that the S. dysenteriae type 1 lipopolysaccharide antigen is specific with respect to the O-antigenic polysaccharide chain.
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PMID:The humoral antibody response to Shigella dysenteriae type 1 infection, as determined by ELISA. 638 7

The requirement for both plasmid and chromosomal genes in the biosynthesis of Shigella dysenteriae 1 lipopolysaccharide O antigen was demonstrated in Escherichia coli-Shigella hybrids. A 6-megadalton S. dysenteriae 1 plasmid, designated pWR23, was phenotypically tagged with the Tn3 ampicillin-resistance transposon. The tagged plasmid, designated pWR24, was transferred by transformation or conjugal mobilization to a rough E. coli K-12 recipient. Although the resultant hybrids were agglutinated in S. dysenteriae 1 antiserum, they did not remove all of the anti-Shiga agglutinins in absorption experiments. Modified lipid A core structure was detected in these hybrids, but Shiga O antigen was not expressed. When the his+ locus of the S. dysenteriae 1 chromosome was transferred by transduction to E. coli K-12 containing pWR24, complete Shiga O antigen was expressed. Lipopolysaccharide extracted from these hybrids was indistinguishable chemically, electrophoretically, and serologically from native S. dysenteriae 1 lipopolysaccharide.
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PMID:Expression of lipopolysaccharide O antigen in Escherichia coli K-12 hybrids containing plasmid and chromosomal genes from Shigella dysenteriae 1. 638 45

Specificity of immune response to smooth and rough mutant strains of Salmonella minnesota was investigated. Immunization of mice with Rd and Re rough mutants resulted in formation of bactericidal plaque-forming cells directed against the lipopolysaccharide structure of both the mutants and the parental smooth strain. These antibody plaques, however, were not bactericidal for smooth strains of other gram-negative species, i.e., Escherichia coli, Salmonella typhosa, Klebsiella pneumoniae, Shigella dysenteriae, and Pseudomonas aeruginosa. Plaques produced against the smooth strain of S. minnesota or other species were not bactericidal for rough strains. It was concluded that immunization with rough mutants produces bactericidal antibodies directed against the closely related parental strain but not against smooth strains of unrelated bacterial species. The relevance of these observations to the nonspecific protection by rough mutants is discussed.
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PMID:Immune response to parental and rough mutant strains of Salmonella minnesota. 679 18


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