Nod2: a key regulator linking microbiota to intestinal mucosal immunity.
Nod2: a key regulator linking microbiota to intestinal mucosal immunity.
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DOI：
10.1007/s00109-011-0802-y
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发表时间：
2012-01
影响因子：
4.7
通讯作者：
Kobayashi, Koichi S.
中科院分区：
文献类型：
--
作者：
Biswas, Amlan;Petnicki-Ocwieja, Tanja;Kobayashi, Koichi S.
人体肠道内有大量的细菌，这些细菌不断与肠道免疫系统相互作用，引发非病理性的基础水平免疫应答。越来越多的证据表明肠道微生物群的生态失调是炎症性肠病易感性的潜在因素。NOD2的功能缺失突变是与回肠克罗恩病相关的较强遗传因素之一。事实上，Nod2是肠道微生物群的关键调节因子，因为在Nod2缺陷小鼠中末端回肠中的微生物群失调。Nod2在潘氏细胞中高度表达，潘氏细胞负责通过抗微生物化合物调节回肠微生物菌群，并且Nod2缺陷的回肠肠上皮不能有效地杀死细菌。因此，克罗恩病中的NOD2突变可能通过改变回肠微生物群和粘膜免疫之间的相互作用来增加疾病易感性。
The human intestine harbors a large number of bacteria that are constantly interacting with the intestinal immune system, eliciting non-pathological basal level immune responses. Increasing evidence points to dysbiosis of microbiota in the intestine as an underlying factor in inflammatory bowel disease susceptibility. Loss of function mutations in NOD2 are among the stronger genetic factors linked to ileal Crohn’s disease. Indeed, Nod2 is a key regulator of microbiota in the intestine, as microflora in the terminal ileum is dysregulated in Nod2-deficient mice. Nod2 is highly expressed in Paneth cells, which are responsible for the regulation of ileal microflora by anti-microbial compounds, and Nod2-deficient ileal intestinal epithelia are unable to kill bacteria efficiently. It is therefore likely that NOD2 mutations in Crohn’s disease may increase disease susceptibility by altering interactions between ileal microbiota and mucosal immunity.
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