Gastric mucosal response to Helicobacter pylori

Hidekazu Suzuki, Tatsuhiro Masaoka, Masaharu Miyazawa, Masayuki Suzuki, Soichiro Miura, Hiromasa Ishii

研究成果: Article査読

14 被引用数 (Scopus)

抄録

Since Marshall's discovery before 20 years, Helicobacter pylori (H. pylori) infection is reportedly to be associated with a variety of clinical outcomes including peptic ulcer disease and gastric cancer. The first step of the H. pylori colonization might be its adhesion to the surface epithelial cells, which evokes gastric inflammatory events initiated by neutrophil recruitment from the microcirculation. Mongolian gerbil is one of the suitable animal models for H. pylori infection, which exerts gastric ulcer and cancer with its bacterial infection. In H. pylori-colonized gerbils, extensive levels of microvascular leukocyte adhesion and migration into the parenchymal side and significant levels of inflammatory cell infiltration are encountered. Bacterial urease not only neutralizes gastric luminal acid, but also plays as an adhesion factor to the surface epithelium. Recently, such an adhesion to the epithelium is reported to be important for bacterial type IV secretory system, which intermediates Cag A injection into the epithelial cells. Then, multiple chemokine and cytokine networks are activated and mucosal inflammatory lesion formation would be completed. In the long-term colonization of H. pylori, gastric mucosal cell turnover would be modified due to persistent inflammation and then such deregulation of cell turnover might link to the precancerous lesion formation.

本文言語English
ページ(範囲)40-44
ページ数5
ジャーナルKeio Journal of Medicine
51
SUPPL. 2
DOI
出版ステータスPublished - 2002 12月

ASJC Scopus subject areas

  • 医学(全般)

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