Article ID Journal Published Year Pages File Type
6096566 Gastroenterology 2010 14 Pages PDF
Abstract
TcdA and TcdB trigger IL-1β release by activating an ASC-containing inflammasome, a response that contributes to toxin-induced inflammation and damage in vivo. Pretreating mice with the IL-1 receptor antagonist anakinra afforded the same level of protection that was observed in ASC−/− mice. These data suggest that targeting inflammasome or IL-1β signaling may represent new therapeutic targets in the treatment of CDAD.
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