イタノ ナオキ
ITANO NAOKI
板野 直樹 所属 京都産業大学 生命科学部 先端生命科学科 職種 教授 |
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言語種別 | 英語 |
発行・発表の年月 | 2009/04 |
形態種別 | 研究論文 |
査読 | 査読あり |
標題 | Role of ASC in the Mouse Model of Helicobacter pylori Infection |
執筆形態 | その他 |
掲載誌名 | JOURNAL OF HISTOCHEMISTRY & CYTOCHEMISTRY |
出版社・発行元 | HISTOCHEMICAL SOC INC |
巻・号・頁 | 57(4),pp.327-338 |
著者・共著者 | Bekale N. Benoit,Motohiro Kobayashi,Masatomo Kawakubo,Michiko Takeoka,Kenji Sano,Jian Zou,Naoki Itano,Hiroko Tsutsui,Tetsuo Noda,Minoru Fukuda,Jun Nakayama,Shun'ichiro Taniguchi |
概要 | Apoptosis-associated speck-like protein containing a C-terminal caspase recruitment domain (ASC) is an adaptor molecule activating caspase-1 that stimulates prointerleukin-1 beta (pro-IL-1 beta) and pro-IL-18, two pro-inflammatory cytokines with critical functions in host defense against a variety of pathogens. In this study, we investigated the role of ASC in the host defense against Helicobacter pylori utilizing ASC-deficient mice. Mice were orally inoculated with H. pylori; bacterial load, degree of gastritis, and mucosal levels of inflammatory cytokines were analyzed and compared with those obtained from wild-type mice. We found more prominent H. pylori colonization in ASC-deficient mice, as revealed by colony-forming unit counts. Both groups of mice developed gastritis; however, ASC-deficient mice showed significant attenuation of inflammation despite high H. pylori colonization. ELISA, immunohistochemistry, and quantitative RT-PCR analyses revealed complete suppression of IL-1 beta and IL-18, and substantial reduction of interferon-gamma (IFN-gamma) expression, in ASC-deficient mice without apparent upregulation of other cytokines, including IL-10 and tumor necrosis factor-alpha. These results as a whole indicate that ASC exerts considerable influence on the host defense, acting through IL-1 beta/IL-18 and subsequent IFN-gamma production, which in turn contributes to continuous chronic inflammatory response and consequent reduction of H. pylori colonization. (J Histochem Cytochem 57:327-338, 2009) |
DOI | 10.1369/jhc.2008.952366 |
ISSN | 0022-1554 |