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Pathogenesis of Helicobacter pylori Infection
Author(s) -
Hatakeyama Masanori,
Brzozowski Tomasz
Publication year - 2006
Publication title -
helicobacter
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.206
H-Index - 79
eISSN - 1523-5378
pISSN - 1083-4389
DOI - 10.1111/j.1478-405x.2006.00424.x
Subject(s) - caga , helicobacter pylori , biology , proinflammatory cytokine , carcinogenesis , atrophic gastritis , tlr2 , immunology , pathogenesis , pathogenicity island , cancer research , cancer , gastritis , gene , inflammation , tlr4 , genetics , virulence
Much interest has been shown in the relationship between Helicobacter pylori infection and gastric carcinogenesis. It is becoming clearer that H. pylori strains carrying a functional cag pathogenicity island ( cag PAI), which encodes the type IV secretion system (TFSS) and its effector CagA, play an important role in the development of gastric carcinoma. Furthermore, genetic polymorphism present in the cag A gene appears to influence the degree of an individual cag PAI‐positive H. pylori to elicit gastric mucosal lesions, and this process is significantly affected by host genetic polymorphisms such as proinflammatory cytokine gene polymorphisms. Pathomechanism of gastric carcinogenesis associated with H. pylori includes bacteria–host interaction leading to morphologic alterations such as atrophic gastritis and gastrointestinal metaplasia mediated by COX‐2 overexpression, cancer cell invasion, and neo‐angiogenesis via TLR2/TLR9 system and transcription factors (e.g., NF‐κB) activation. In addition, H. pylori infection triggers adhesion molecule expression and activity and produces an enhancement in oxidative stress interacting with gastric production of appetite hormone ghrelin and nonsteroidal anti‐inflammatory drugs.