The interaction of host genetic factors and Helicobacter pylori infection

T. Ando, Y. Goto, K. Ishiguro, O. Maeda, O. Watanabe, Naoki Omiya, Y. Niwa, N. Hamajima, E. El-Omar, H. Goto

Research output: Contribution to journalReview article

19 Citations (Scopus)

Abstract

Helicobacter pylori plays an important role in the development of atrophic gastritis that represents the most recognized pathway in multistep gastric carcinogenesis. Recent studies suggest that a combination of host genetic factors, bacterial virulence factors, and environmental and lifestyle factors determine the severity of gastric damage and the eventual clinical outcome of Helicobacter pylori infection. As to bacterial virulence factors, a high proportion of Japanese strains are cagA+vacAs1. The CagA protein is injected from attached Helicobacter pylori into gastric epithelial cells and the CagA-SHP-2 interactions elicit cellular changes that increase the risk of carcinogenesis. Host cytokine gene polymorphisms and a frequent single nucleotide polymorphism in the PTPN11 gene that encodes SHP-2 may associate with gastric atrophy among Helicobacter pylori-infected subjects. Prevention of gastric cancer requires the development of better screening strategies for determining eradication candidates and further improvement of treatments of Helicobacter pylori infection.

Original languageEnglish
Pages (from-to)10-14
Number of pages5
JournalInflammopharmacology
Volume15
Issue number1
DOIs
Publication statusPublished - 01-02-2007
Externally publishedYes

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Helicobacter Infections
Helicobacter pylori
Stomach
Virulence Factors
Carcinogenesis
Atrophic Gastritis
Genes
Stomach Neoplasms
Atrophy
Single Nucleotide Polymorphism
Life Style
Epithelial Cells
Cytokines
Proteins

All Science Journal Classification (ASJC) codes

  • Immunology
  • Pharmacology
  • Pharmacology (medical)

Cite this

Ando, T., Goto, Y., Ishiguro, K., Maeda, O., Watanabe, O., Omiya, N., ... Goto, H. (2007). The interaction of host genetic factors and Helicobacter pylori infection. Inflammopharmacology, 15(1), 10-14. https://doi.org/10.1007/s10787-006-1556-y
Ando, T. ; Goto, Y. ; Ishiguro, K. ; Maeda, O. ; Watanabe, O. ; Omiya, Naoki ; Niwa, Y. ; Hamajima, N. ; El-Omar, E. ; Goto, H. / The interaction of host genetic factors and Helicobacter pylori infection. In: Inflammopharmacology. 2007 ; Vol. 15, No. 1. pp. 10-14.
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Ando, T, Goto, Y, Ishiguro, K, Maeda, O, Watanabe, O, Omiya, N, Niwa, Y, Hamajima, N, El-Omar, E & Goto, H 2007, 'The interaction of host genetic factors and Helicobacter pylori infection', Inflammopharmacology, vol. 15, no. 1, pp. 10-14. https://doi.org/10.1007/s10787-006-1556-y

The interaction of host genetic factors and Helicobacter pylori infection. / Ando, T.; Goto, Y.; Ishiguro, K.; Maeda, O.; Watanabe, O.; Omiya, Naoki; Niwa, Y.; Hamajima, N.; El-Omar, E.; Goto, H.

In: Inflammopharmacology, Vol. 15, No. 1, 01.02.2007, p. 10-14.

Research output: Contribution to journalReview article

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AU - Ando, T.

AU - Goto, Y.

AU - Ishiguro, K.

AU - Maeda, O.

AU - Watanabe, O.

AU - Omiya, Naoki

AU - Niwa, Y.

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AU - El-Omar, E.

AU - Goto, H.

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AB - Helicobacter pylori plays an important role in the development of atrophic gastritis that represents the most recognized pathway in multistep gastric carcinogenesis. Recent studies suggest that a combination of host genetic factors, bacterial virulence factors, and environmental and lifestyle factors determine the severity of gastric damage and the eventual clinical outcome of Helicobacter pylori infection. As to bacterial virulence factors, a high proportion of Japanese strains are cagA+vacAs1. The CagA protein is injected from attached Helicobacter pylori into gastric epithelial cells and the CagA-SHP-2 interactions elicit cellular changes that increase the risk of carcinogenesis. Host cytokine gene polymorphisms and a frequent single nucleotide polymorphism in the PTPN11 gene that encodes SHP-2 may associate with gastric atrophy among Helicobacter pylori-infected subjects. Prevention of gastric cancer requires the development of better screening strategies for determining eradication candidates and further improvement of treatments of Helicobacter pylori infection.

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