Novel players in inflammatory bowel disease pathogenesis.
Novel players in inflammatory bowel disease pathogenesis.
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DOI：
10.1007/s11894-012-0250-z
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发表时间：
2012-04
影响因子：
--
通讯作者：
Boone, David L
中科院分区：
文献类型：
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作者：
Murphy, Stephen F;Kwon, John H;Boone, David L
炎症性肠病研究中的技术和概念进步揭示了导致这些疾病发病的新机制。越来越清楚的是，肠道的微生物群和肠道细胞对微生物群的反应可以引发或导致肠道炎症。来自遗传学研究的证据已经确定了IBD相关基因，这些基因与自噬和微生物的先天感应有关。这些基因也在宿主-微生物相互作用界面的细胞类型-潘氏细胞的体内平衡中发挥关键作用。在这里，我们讨论了最近的研究结果，强调了微生物组，潘氏细胞和自噬在炎症性肠病中的重要性。
Technological and conceptual advances in inflammatory bowel disease research have uncovered new mechanisms that contribute to the pathogenesis of these disorders. It is becoming increasingly clear that the microbiota of the gut and the response of intestinal cells to that microbiota can initiate or contribute to intestinal inflammation. Evidence from genetic studies have identified IBD-associated genes implicated in autophagy and innate sensing of microbes. These genes also play key roles in the homeostasis of a cell type that stands at the interface of host-microbial interaction – the Paneth cell. Here we discuss recent findings that underscore the importance of the microbiome, Paneth cells and autophagy in inflammatory bowel disease.