| Theme | Gastrointestinal Diseases and Cytokines : Pathophysiological Control | |
|---|---|---|
| Title | Helicobacter pylori and Cytokines : Bacterial Colonization, Gastritis, and Gastric Cancer | |
| Publish Date | 2005/03 | |
| Author | Hiroaki Murata | Department of Internal Medicine and Therapeutics, Osaka University Graduate School of Medicine |
| Author | Shingo Tsuji | Department of Internal Medicine and Therapeutics, Osaka University Graduate School of Medicine |
| Author | Masahiko Tsujii | Department of Internal Medicine and Therapeutics, Osaka University Graduate School of Medicine |
| Author | Hiroshi Eguchi | Department of Clinical Laboratory Science, School of Allied Health Sciences, Osaka University Graduate School of Medicine |
| Author | Kayoko Asahi | Department of Clinical Laboratory Science, School of Allied Health Sciences, Osaka University Graduate School of Medicine |
| Author | Sunao Kawano | Department of Clinical Laboratory Science, School of Allied Health Sciences, Osaka University Graduate School of Medicine |
| [ Summary ] | Helicobacter pylori (H. pylori) colonizes the human gastric mucosa and induces a variety of cytokines and their related products. Inrerleukins (ILs) such as IL-8 and IL-1β, tumor necrosis factor(TNF)-α and interferon (IFN)-γ etc. are produced, and Th 1-predominant immune response are elicited, resulting in chronic gastritis. On the other hand, the Th 2 immune responses attenuate gastritis and inhibit the colonization and growth of the bacteria. IL-8 activates transcription factors, such as nuclear factor(NF)-κB, not the cagA gene- but the cag-pathogenicity island (cag-PAI) -dependently, and recruits polymorphonuclear cells into the gastric mucosa to aggravate gastritis. As host factors, single nucleotide polymorphisms (SNPs) in IL-1β, IL-1 receptor antagonist (IL-1 RN), TNF-α, and IL-10 are known to produce a high risk of hypochlorhydria, gastric mucosal atrophy, and gastric cancer. This review describes the significance of a variety of cytokines and their related products induced by H. pylori and the molecular mechanisms underlying the pathogenesis of the organism. | |