Redox signaling regulates commensal-mediated mucosal homeostasis and restitution and requires formyl peptide receptor 1.
Redox signaling regulates commensal-mediated mucosal homeostasis and restitution and requires formyl peptide receptor 1.
复制标题
作者：
哺乳动物肠道微生物群对于正常的肠道发育、更新和修复至关重要。肠粘膜损伤可发生在感染、手术创伤和特发性炎症性肠病中。粘膜损伤的修复，称为复原，以及肠内稳态的恢复涉及肠上皮细胞的诱导和协调的增殖和迁移。N-甲酰基肽受体（FPRs）是广泛表达的模式识别受体，其可以特异性结合并诱导对宿主衍生的和细菌的肽和小分子的反应。在这里，我们报告了肠道微生物群的特定成员刺激肠上皮细胞上的FPR 1通过肠细胞NADPH氧化酶NOX 1产生活性氧，导致粘着斑激酶（FAK）和ERK MAPK的快速磷酸化。这些事件刺激邻近结肠伤口的肠细胞的迁移和增殖。总之，这些发现确定了FPR 1作为模式识别受体的新作用，用于感知肠道微生物群，通过肠细胞NOX 1产生ROS促进粘膜伤口的修复。
The mammalian gut microbiota is essential for normal intestinal development, renewal and repair. Injury to the intestinal mucosa can occur with infection, surgical trauma, and in idiopathic inflammatory bowel disease. Repair of mucosal injury, termed restitution, as well as restoration of intestinal homeostasis involves induced and coordinated proliferation and migration of intestinal epithelial cells. N-formyl peptide receptors (FPRs) are widely expressed pattern recognition receptors that can specifically bind and induce responses to host derived and bacterial peptides and small molecules. Here we report that specific members of the gut microbiota stimulate FPR1 on intestinal epithelial cells to generate reactive oxygen species via enterocyte NADPH oxidase NOX1, causing rapid phosphorylation of Focal Adhesion Kinase (FAK) and ERK MAPK. These events stimulate migration and proliferation of enterocytes adjacent to colonic wounds. Together, these findings identify a novel role of FPR1 as pattern recognition receptors for perceiving the enteric microbiota that promotes repair of mucosal wounds via generation of ROS from the enterocyte NOX1.
登录
查看更多内容
DOI：
10.1161/atvbaha.112.249508
发表时间：
2012-08
期刊：
Arteriosclerosis, thrombosis, and vascular biology
影响因子：
--
作者：
Norling LV;Dalli J;Flower RJ;Serhan CN;Perretti M
通讯作者：
Perretti M
影响因子：
4.4
作者：
Babbin, Brian A.;Jesaitis, Algirdas J.;Nusrat, Asma
通讯作者：
Nusrat, Asma
DOI：
10.1073/pnas.0803343106
发表时间：
2009-01-06
影响因子：
11.1
作者：
Seno, Hiroshi;Miyoshi, Hiroyuki;Stappenbeck, Thaddeus S.
通讯作者：
Stappenbeck, Thaddeus S.
影响因子：
5.3
作者：
Coant, Nicolas;Ben Mkaddem, Sanae;Ogier-Denis, Eric
通讯作者：
Ogier-Denis, Eric
影响因子：
3.7
作者：
Bylund, J;Samuelsson, M;Karlsson, A
通讯作者：
Karlsson, A