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Genomic-equence comparison of two unrelated isolates of the human gastric pathogen Helicobacter pylori
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Kersulyte D, Chalkauskas H, Berg DE. Emergence of recombinant strains of Helicobacter pylori during human infection. Mol Microbiol 1999; 31:31-43. Elegant study that shows that multiple recombination events had occurred during chronic colonization of a patient with two H. pylori strains and that those recombination events had given rise to at least six different recombinant H. pylori strains. Some of those had eliminated the cag pathogenicity island by recombination with 'cag empty site' DNA from a cag-negative strain.
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Kersulyte, D.1
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Marshall DG, Dundon WG, Beesley SM, Smyth CJ. Helicobacter pylori-a conundrum of genetic diversity. Microbiology 1998; 144:2925-2939. A well-written extensive review of studies describing diversity of H. pylori strains.
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Suerbaum, S.1
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Josenhans C, Ferrera RL, Labigne A, Suerbaum S. Cloning and allelic exchange mutagenesis of two flagellin genes from Helicobacter felis. Mol Microbiol 1999; 33:350-362. First study to demonstrate genetic manipulation of Helicobacter felis. flaA mutants of H. felis were unable to colonize mice. The authors also provide evidence that H. felis flagellins are glycosylated.
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Mol Microbiol
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Spohn G, Scarlato V. Motility of Helicobacter pylori is coordinately regulated by the transcriptional activator FlgR, an NtrC homolog. J Bacteriol 1999; 181:593-599. The first characterization of a transcriptional regulator (flgR) in H. pylori.
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Schmitz A, Josenhans C, Suerbaum S. Cloning and characterization of the Helicobacter pylori flbA gene, which codes for a membrane protein involved in coordinated expression of flagellar genes. J Bacteriol 1997; 179:987-997.
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McGee DJ, May CA, Garner RM, Himpsl JM, Mobley HL. Isolation of Helicobacter pylori genes that modulate urease activity. J Bacteriol 1999; 181:2477-2484. The authors identify genes that reduce or increase H. pylori urease activity in an E. coli background. Among the genes that reduce urease activity is the flagellar regulatory gene, flbA.
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J Bacteriol
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Skouloubris S, Thiberge JM, Labigne A, De Reuse H. The Helicobacter pylori Urel protein is not involved in urease activity but is essential for bacterial survival in vivo. Infect Immun 1998; 66:4517-4521. A clear-cut study showing that Urel protein, in contrast to previous reports, is not required for urease activity, but is essential for colonization.
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Skouloubris, S.1
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Essential role of Helicobacter pylori gamma-glutamyltranspeptidase for the colonization of the gastric mucosa of mice
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Chevalier C, Thiberge JM, Ferrero RL, Labigne A. Essential role of Helicobacter pylori gamma-glutamyltranspeptidase for the colonization of the gastric mucosa of mice. Mol Microbiol 1999; 31:1359-1372. A straightforward study that shows that gammaglutamyl transpeptidase (GGT) is essential for colonization in mice, but non-essential for growth in vitro.
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Mol Microbiol
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Guruge JL, Falk PG, Lorenz RG, Dans M, Wirth HP, Blaser MJ, et al. Epithelial attachment alters the outcome of Helicobacter pylori infection. Proc Natl Acad Sci U.S.A. 1998; 95:3925-3930. Authors use a transgenic mouse model to study the role of Lewis b antigen as a binding site for H. pylori and the role of adhesion for disease induction. The study shows that bacteria that adhere to gastric epithelium will cause more gastritis and induce parietal cell loss.
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Guruge, J.L.1
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Syder AJ, Guruge JL, Li Q, Hu Y, Oleksiewicz CM, Lorenz RG, et al. Helicobacter pylori attaches to NeuAc α 2,3Gal β 1,4 glycoconjugates produced in the stomach of transgenic mice lacking parietal cells. Mol Cell 1999; 3:263-274. Another elegant study showing the potential of transgenic mice models for elucidating the role of adherence to specific receptors in H. pylori associated disease.
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Su B, Hellstrom PM, Rubio C, Celik J, Granstrom M, Normark S. Type I Helicobacter pylori shows Lewis(b)-independent adherence to gastric cells requiring de novo protein synthesis in both host and bacteria. J Infect Dis 1998; 178:1379-1390. Binding of H. pylori to gastric cells was reduced by inhibition of either bacterial or eukaryotic protein synthesis.
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Su, B.1
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The interrelationship between Helicobacter pylori vacuolating cytotoxin and gastric carcinoma
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University of Helicobacter pylori vacA and cagA genes and relationship to VacA and CagA protein expression, cytotoxin production, and associated diseases
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Rudi J, Kolb C, Maiwald M, Kuck D, Sieg A, Galle PR, Stremmel W. University of Helicobacter pylori vacA and cagA genes and relationship to VacA and CagA protein expression, cytotoxin production, and associated diseases. J Clin Microbiol 1998; 36:944-948. Sixty-five H. pylori strains were isolated from dyspeptic patients. vacA s1 was found to be associated with occurrence of peptic ulceration and presence of cagA, cytotoxin activity, and VacA expression.
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J Clin Microbiol
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Yang JC, Kuo CH, Wang HJ, Wang TC, Chang CS, Wang WC. Vacuolating toxin gene polymorphism among Helicobacter pylori clinical isolates and its association with m1, m2, or chimeric vacA middle types. Scand J Gastroenterol 1998; 33:1152-1157. Specific vacA alleles are believed to be associated with increased virulence. 89 isolates examined with RFLP of the 2kb PCR amplified vacA middle region. 28 distinct vacA RFLPs seen among the 89 isolates.
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Scand J Gastroenterol
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de Bernard M, Moschioni M, Papini E, Telford JL, Rappuoli R, Montecucco C. TPA and butyrate increase cell sensitivity to the vacuolating toxin of Helicobacter pylori. Febs Letters 1998; 436:218-222.
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Pai R, Wyle FA, Cover TL, Itani RM, Domek MJ, Tarnawski AS. Helicobacter pylori culture supernatant interferes with epidermal growth factor-activated signal transduction in human gastric KATO III cells. Am J Pathol 1998; 152:1617-1624. VacA interferes with EGF activated signal transduction pathways, which are known to be essential for cell proliferation and ulcer healing.
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