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The inflamatory activity in Helicobacter pylori infection is predominantly organism related

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Helicobacter pylori
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Abstract

Helicobacter pylori is remarkably adapted to survival in its niche on the surface of the human gastric mucosa. It persists for decades with minimal damage in the majority of those infected. Nevertheless, infection is almost invariably associated with some degree of chronic active gastritis. The intensity of this inflammation of the gastric mucosa has been correlated with the risk of developing complications of the infection such as peptic ulcer, and the inflammation invariably abates after successful elimination of the infection. To modulate the host response, H. pylori has evolved a complex set of genes. Recent genetic studies contributed to defining the function of some of these genes. In addition, these studies, as well as the analysis of the two complete genomes of H. pylori, have provided important information regarding the mechanisms by which H. pylori modulates gene expression. Gene regulation allows the pathogen to further adapt to its environment and to further modulate its relationship to its host, including inflammation.

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References

  1. Segal ED, Falkow S, Tompkins LS. Helicobacter pylori attachment to gastric cells induces cytoskeletal rearrangements and tyrosine phosphorylation of host cell proteins. Proc Natl Acad Sci USA. 1996;93:1259–1264.

    Article  PubMed  CAS  Google Scholar 

  2. Keates S, Hitti YS, Upton M, Kelly CP. Helicobacter pylori infection activates NF-kappa B in gastric epithelial cells. Gastroenterology. 1997;113:1099–1109.

    Article  PubMed  CAS  Google Scholar 

  3. Iiver D, Arnqvist A, Ogren J et al. Helicobacter pylori adhesin binding fucosylated histo-blood group antigens revealed by retagging. Science. 1998;279:373–377.

    Article  Google Scholar 

  4. Guruge JL, Falk PG, Lorenz RG et al. Epithelial attachment alters the outcome of Helicobacter pylori infection. Proc Natl Acad Sci USA. 1998;95:3925–3930.

    Article  PubMed  CAS  Google Scholar 

  5. Gerhard M, Lehn N, Neumayer N et al. Clinical relevance of the Helicobacter pylori gene for blood-group antigen-binding adhesin. Proc Natl Acad Sci USA. 1999;96:12778–12783.

    Article  PubMed  CAS  Google Scholar 

  6. Syder AJ, Guruge JL, Li Q et al. Helicobacter pylori attaches to NeuAc alpha 2,3Gal beta 1,4 glycoconjugates produced in the stomach of transgenic mice lacking parietal cells. Mol Cell. 1999;3:263–274.

    Article  PubMed  CAS  Google Scholar 

  7. Odenbreit S, Till M, Hofreuter D, Faller G, Haas R. Genetic and functional characterization of the alpAB gene locus essential for the adhesion of Helicobacter pylori to human gastric tissue. Mol Microbiol. 1999;31:1537–1548.

    Article  PubMed  CAS  Google Scholar 

  8. Cunningham MD, Seachord C, Ratcliffe K, Bainbridge B, Aruffo A, Darveau RP. Helicobacter pylori and Porphyromonas gingivalis lipopolysaccharides are poorly transferred to recombinant soluble CD14. Infect Immun. 1996;64:3601–3608.

    PubMed  CAS  Google Scholar 

  9. Kirkland T, Viriyakosol S, Perez-Perez GI, Blaser MJ. Helicobacter pylori lipopolysaccha-ride can activate 70Z/3 cells via CD14. Infect Immun. 1997;65:604–608.

    PubMed  CAS  Google Scholar 

  10. Semeraro N, Montemurro P, Piccoli C et al. Effect of Helicobacter pylori lipopolysaccharide (LPS) and LPS derivatives on the production of tissue factor and plasminogen activator inhibitor type 2 by human blood mononuclear cells. J Infect Dis. 1996;174:1255–1260.

    Article  PubMed  CAS  Google Scholar 

  11. Sakagami T, Vella J, Dixon MF et al. The endotoxin of Helicobacter pylori is a modulator of host-dependent gastritis. Infect Immun. 1997;65:3310–3316.

    PubMed  CAS  Google Scholar 

  12. Wirth HP, Yang M, Peek RM, Jr, Tham KT, Blaser MJ. Helicobacter pylori Lewis expression is related to the host Lewis phenotype. Gastroenterology. 1997;113:1091–1098.

    Article  PubMed  CAS  Google Scholar 

  13. de Figueiredo Soares T, de Magalhaes Queiroz DM, Mendes EN et al. The interrelationship between Helicobacter pylori vacuolating cytotoxin and gastric carcinoma. Am J Gastroenterol. 1998;93:1841–1847.

    PubMed  Google Scholar 

  14. Rudi J, Kolb C, Maiwald M et al. Diversity of Helicobacter pylori vacA and cagA genes and relationship to VacA and CagA protein expression, cytotoxin production, and associated diseases (see comments). J Clin Microbiol. 1998;36:944–948.

    PubMed  CAS  Google Scholar 

  15. 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 ml, m2, or chimeric vacA middle types. Scand J Gastroenterol. 1998;33:1152–1157.

    Article  PubMed  CAS  Google Scholar 

  16. Miehlke S, Meining A, Morgner A et al. Frequency of vacA genotypes and cytotoxin activity in Helicobacter pylori associated with low-grade gastric mucosa-associated lymphoid tissue lymphoma. J Clin Microbiol. 1998;36:2369–2370.

    PubMed  CAS  Google Scholar 

  17. Yamaoka Y, Kodama T, Kita M, Imanishi J, Kashima K, Graham DY. Relationship of vacA genotypes of Helicobacter pylori to cagA status, cytotoxin production, and clinical outcome. Helicobacter. 1998;3:241–243.

    Article  PubMed  CAS  Google Scholar 

  18. Pagliaccia C, de Bernard M, Lupetti P et al. The m2 form of the Helicobacter pylori cytotoxin has cell type-specific vacuolating activity. Proc Natl Acad Sci USA. 1998;95:10212–10217.

    Article  PubMed  CAS  Google Scholar 

  19. Massari P, Manetti R, Burroni D et al. Binding of the Helicobacter pylori vacuolating cytotoxin to target cells. Infect Immun. 1998;66:3981–3984.

    PubMed  CAS  Google Scholar 

  20. Sommi P, Ricci V, Fiocca R et al. Persistence of Helicobacter pylori VacA toxin and vacuolating potential in cultured gastric epithelial cells. Am J Physiol. 1998;275:G681–868.

    PubMed  CAS  Google Scholar 

  21. de Bernard M, Burroni D, Papini E, Rappuoli R, Telford J, Montecucco C. Identification of the Helicobacter pylori VacA toxin domain active in the cell cytosol. Infect Immun. 1998;66:6014–6016.

    PubMed  Google Scholar 

  22. 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.

    PubMed  CAS  Google Scholar 

  23. Papini E, Satin B, Norais N et al. Selective increase of the permeability of polarized epithelial cell monolayers by Helicobacter pylori vacuolating toxin. J Clin Invest. 1998;102:813–820.

    Article  PubMed  CAS  Google Scholar 

  24. Molinari M, Salio M, Galli C et al. Selective inhibition of Ii-dependent antigen presentation by Helicobacter pylori toxin VacA. J Exp Med. 1998;187:135–140.

    Article  PubMed  CAS  Google Scholar 

  25. Sutton P, Wilson J, Genta R et al. A genetic basis for atrophy: dominant non-responsiveness and Helicobacter induced gastritis in F(l) hybrid mice (See comments). Gut. 1999;45:335–340.

    Article  PubMed  CAS  Google Scholar 

  26. Wirth HP, Beins MH, Yang M, Tham KT, Blaser MJ. Experimental infection of Mongolian gerbils with wild-type and mutant Helicobacter pylori strains. Infect Immun. 1998;66:4856–4866.

    PubMed  CAS  Google Scholar 

  27. Gunn MC, Stephens JC, Stewart JA, Rathbone BJ, West KP. The significance of cagA and vacA subtypes of Helicobacter pylori in the pathogenesis of inflammation and peptic ulceration. J Clin Pathol. 1998;51:761–764.

    Article  PubMed  CAS  Google Scholar 

  28. Glocker E, Lange C, Covacci A, Bereswill S, Kist M, Pahl HL. Proteins encoded by the cag pathogenicity island of Helicobacter pylori are required for NF-kappaB activation. Infect Immun. 1998;66:2346–2348.

    PubMed  CAS  Google Scholar 

  29. Akopyants NS, Clifton SW, Kersulyte D et al. Analyses of the cag pathogenicity island of Helicobacter pylori. Mol Microbiol. 1998;28:37–53.

    Article  PubMed  CAS  Google Scholar 

  30. Crabtree JE, Kersulyte D, Li SD, Lindley IJ, Berg DE. Modulation of Helicobacter pylori induced interleukin-8 synthesis in gastric epithelial cells mediated by cag PAI encoded VirD4 homologue. J Clin Pathol. 1999;52:653–657.

    Article  PubMed  CAS  Google Scholar 

  31. Odenbreit S, Puls J, Sedlmaier B, Gerland E, Fischer W, Haas R. Translocation of Helicobacter pylori CagA into gastric epithelial cells by type IV secretion. Science. 2000;287:1497–1500.

    Article  PubMed  CAS  Google Scholar 

  32. Segal ED, Cha J, Lo J, Falkow S, Tompkins LS. Altered states: involvement of phosphorylated CagA in the induction of host cellular growth changes by Helicobacter pylori. Proc Natl Acad Sci USA. 1999;96:14559–14564.

    Article  PubMed  CAS  Google Scholar 

  33. Peek RM Jr, Thompson SA, Donahue JP et al. Adherence to gastric epithelial cells induces expression of a Helicobacter pylori gene, iceA, that is associated with clinical outcome. Proc Assoc Am Phys. 1998;110:531–544.

    PubMed  CAS  Google Scholar 

  34. Nishiya D, Shimoyama T, Fukuda S, Yoshimura T, Tanaka M, Munakata A. Evaluation of the clinical relevance of the iceA1 gene in patients with Helicobacter pylori infection in Japan. Scand J Gastroenterol. 2000;35:36–39.

    Article  PubMed  CAS  Google Scholar 

  35. van Doom LJ, Figueiredo C, Sanna R et al. Clinical relevance of the cagA, vacA, and iceA status of Helicobacter pylori. Gastroenterology. 1998;115:58–66.

    Article  Google Scholar 

  36. Akopyants NS, Fradkov A, Diatchenko L et al. PCR-based subtractive hybridization and differences in gene content among strains of Helicobacter pylori. Proc Natl Acad Sci USA. 1998;95:13108–13113.

    Article  PubMed  CAS  Google Scholar 

  37. Achtman M, Azuma T, Berg DE et al. Recombination and clonal groupings within Helicobacter pylori from different geographical regions. Mol Microbiol. 1999;32:459–470.

    Article  PubMed  CAS  Google Scholar 

  38. Suerbaum S, Smith JM, Bapumia K et al. Free recombination within Helicobacter pylori. Proc Natl Acad Sci USA. 1998;95:12619–12624.

    Article  PubMed  CAS  Google Scholar 

  39. Kersulyte D, Chalkauskas H, Berg DE. Emergence of recombinant strains of Helicobacter pylori during human infection. Mol Microbiol. 1999;31:31–43.

    Article  PubMed  CAS  Google Scholar 

  40. Spohn G, Beier D, Rappuoli R, Scarlato V. Transcriptional analysis of the divergent cagAB genes encoded by the pathogenicity island of Helicobacter pylori. Mol Microbiol. 1997;26:361–372.

    Article  PubMed  CAS  Google Scholar 

  41. Wang G, Rasko DA, Sherburne R, Taylor DE. Molecular genetic basis for the variable expression of Lewis Y antigen in Helicobacter pylori: analysis of the alpha (1,2) fucosyltrans-ferase gene. Mol Microbiol. 1999;31:1265–1274.

    Article  PubMed  CAS  Google Scholar 

  42. McGowan CC, Necheva A, Thompson SA, Cover TL, Blaser MJ. Acid-induced expression of an LPS-associated gene in Helicobacter pylori. Mol Microbiol. 1998;30:19–31.

    Article  PubMed  CAS  Google Scholar 

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© 2000 Springer Science+Business Media Dordrecht

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Michetti, P. (2000). The inflamatory activity in Helicobacter pylori infection is predominantly organism related. In: Hunt, R.H., Tytgat, G.N.J. (eds) Helicobacter pylori. Springer, Dordrecht. https://doi.org/10.1007/978-94-011-3927-4_21

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  • DOI: https://doi.org/10.1007/978-94-011-3927-4_21

  • Publisher Name: Springer, Dordrecht

  • Print ISBN: 978-94-010-5753-0

  • Online ISBN: 978-94-011-3927-4

  • eBook Packages: Springer Book Archive

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