Innate immunity in inflammatory bowel disease: a disease hypothesis.
Innate immunity in inflammatory bowel disease: a disease hypothesis.
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DOI：
10.1002/path.2291
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发表时间：
2008-01
影响因子：
7.3
通讯作者：
Segal, A. W.
中科院分区：
文献类型：
--
作者：
Marks, D. J. B.;Segal, A. W.
克罗恩氏病是由于胃肠道中高度集中的细菌与底层组织之间存在缺陷的相互作用引起的。人们普遍认为，它是由过度活跃的炎症反应或“自身免疫”引起的。最近出现的证据表明，问题是身体对细菌和其他肠道内容物通过肠道粘膜屏障渗透的反应方式失败。克罗恩病并不是由过度炎症引起的，其主要机制实际上是免疫缺陷。炎症介质的产生失败导致中性粒细胞募集不足，导致细菌和其他碎片的清除不足。在某些情况下，这种急性炎症的损害可以通过NOD2的信号来补偿。如果不清除，肠壁中的异物会被巨噬细胞吸收，引发肉芽肿反应和克罗恩病特有的局部和全身后遗症。
Crohn's disease arises from a defective interaction between the highly concentrated mass of bacteria in the gastrointestinal tract and the underlying tissues. It has generally been believed to result from an excessively exuberant inflammatory response or from ‘autoimmunity’. Recent evidence has emerged that the problem is instead a failure of the way in which the body responds to the penetration of bacteria and other bowel contents through the intestinal mucosal barrier. Rather than Crohn's disease being caused by excessive inflammation, the primary mechanism is actually that of an immunodeficiency. Failure of inflammatory mediator production leads to insufficient recruitment of neutrophils, resulting in inadequate removal of bacteria and other debris. This impairment of acute inflammation can be compensated in some circumstances by signalling through NOD2. If not cleared, the foreign material in the bowel wall is taken up within macrophages, eliciting a granulomatous reaction and the local and systemic sequelae so characteristic of Crohn's disease.
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