{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,23]],"date-time":"2026-09-23T14:02:36Z","timestamp":1790172156071,"version":"4.1.0"},"reference-count":47,"publisher":"SAGE Publications","issue":"4","license":[{"start":{"date-parts":[[2008,12,24]],"date-time":"2008-12-24T00:00:00Z","timestamp":1230076800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J Histochem Cytochem."],"published-print":{"date-parts":[[2009,4]]},"abstract":"<jats:p>Apoptosis-associated speck-like protein containing a C-terminal caspase recruitment domain (ASC) is an adaptor molecule activating caspase-1 that stimulates pro-interleukin-1\u03b2 (pro-IL-1\u03b2) 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\u03b2 and IL-18, and substantial reduction of interferon-\u03b3 (IFN-\u03b3) expression, in ASC-deficient mice without apparent upregulation of other cytokines, including IL-10 and tumor necrosis factor-\u03b1. These results as a whole indicate that ASC exerts considerable influence on the host defense, acting through IL-1\u03b2\/IL-18 and subsequent IFN-\u03b3 production, which in turn contributes to continuous chronic inflammatory response and consequent reduction of H. pylori colonization.<\/jats:p>","DOI":"10.1369\/jhc.2008.952366","type":"journal-article","created":{"date-parts":[[2008,12,8]],"date-time":"2008-12-08T20:48:29Z","timestamp":1228769309000},"page":"327-338","source":"Crossref","is-referenced-by-count":21,"title":["Role of ASC in the Mouse Model of\n                    <i>Helicobacter pylori<\/i>\n                    Infection"],"prefix":"10.1177","volume":"57","author":[{"given":"Bekale N.","family":"Benoit","sequence":"first","affiliation":[{"name":"Department of Molecular Oncology, Institute on Aging and Adaptation, Shinshu University Graduate School of Medicine, Matsumoto, 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