臨牀消化器内科 Vol.20 No.3(1)


特集名 消化器疾患とサイトカイン -- 病態制御に向けて
題名 H. pyloriとサイトカイン
発刊年月 2005年 03月
著者 村田 浩昭 大阪大学大学院医学系研究科病態情報内科学
著者 辻 晋吾 大阪大学大学院医学系研究科病態情報内科学
著者 辻井 正彦 大阪大学大学院医学系研究科病態情報内科学
著者 江口 寛 大阪大学大学院保健学専攻機能診断科学
著者 朝日 佳代子 大阪大学大学院保健学専攻機能診断科学
著者 川野 淳 大阪大学大学院保健学専攻機能診断科学
【 要旨 】 Helicobacter pyloriはヒトの胃粘膜に生息し，さまざまなサイトカインやその関連物質産生を誘導する．IL-8, IL-1βなどのインターロイキン，TNF-α, IFN-γなどが産生され，Th 1型優位の免疫反応が惹起されて慢性胃炎が起こる．一方，Th 2型免疫反応は，胃炎を軽減させ，菌の生着，生育を抑制する．IL-8は，cagA遺伝子ではなく, cag-pathogenicity island (cag-PAI) 依存性にNF-κBなどの転写因子を活性化させ，好中球を胃粘膜に遊走させて胃炎を増悪させる．宿主側因子として，IL-1β, IL-1RN, TNF-α, IL-10のSNPがあり，低酸症や胃粘膜萎縮，および胃癌のハイリスク群が存在する．
Theme Gastrointestinal Diseases and Cytokines : Pathophysiological Control
Title Helicobacter pylori and Cytokines : Bacterial Colonization, Gastritis, and Gastric Cancer
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.
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