作者
Simon A Hirota, Jeffrey Ng, Alan Lueng, Maitham Khajah, Ken Parhar, Yan Li, Victor Lam, Mireille S Potentier, Kelvin Ng, Misha Bawa, Donna-Marie McCafferty, Kevin P Rioux, Subrata Ghosh, Ramnik J Xavier, Sean P Colgan, Jurg Tschopp, Daniel Muruve, Justin A MacDonald, Paul L Beck
发表日期
2011/6/1
期刊
Inflammatory bowel diseases
卷号
17
期号
6
页码范围
1359-1372
出版商
Oxford University Press
简介
Background
Attenuated innate immune responses to the intestinal microbiota have been linked to the pathogenesis of Crohn's disease (CD). Recent genetic studies have revealed that hypofunctional mutations of NLRP3, a member of the NOD-like receptor (NLR) superfamily, are associated with an increased risk of developing CD. NLRP3 is a key component of the inflammasome, an intracellular danger sensor of the innate immune system. When activated, the inflammasome triggers caspase-1-dependent processing of inflammatory mediators, such as IL-1β and IL-18.
Methods
In the current study we sought to assess the role of the NLRP3 inflammasome in the maintenance of intestinal homeostasis through its regulation of innate protective processes. To investigate this role, Nlrp3−/− and wildtype mice were assessed in the dextran sulfate sodium and 2,4,6-trinitrobenzenesulfonic …
学术搜索中的文章
SA Hirota, J Ng, A Lueng, M Khajah, K Parhar, Y Li… - Inflammatory bowel diseases, 2011