|  Help  |  About  |  Contact Us

Publication : Distinct Commensals Induce Interleukin-1β via NLRP3 Inflammasome in Inflammatory Monocytes to Promote Intestinal Inflammation in Response to Injury.

First Author  Seo SU Year  2015
Journal  Immunity Volume  42
Issue  4 Pages  744-55
PubMed ID  25862092 Mgi Jnum  J:229698
Mgi Id  MGI:5753014 Doi  10.1016/j.immuni.2015.03.004
Citation  Seo SU, et al. (2015) Distinct Commensals Induce Interleukin-1beta via NLRP3 Inflammasome in Inflammatory Monocytes to Promote Intestinal Inflammation in Response to Injury. Immunity 42(4):744-55
abstractText  The microbiota stimulates inflammation, but the signaling pathways and the members of the microbiota involved remain poorly understood. We found that the microbiota induces interleukin-1beta (IL-1beta) release upon intestinal injury and that this is mediated via the NLRP3 inflammasome. Enterobacteriaceae and in particular the pathobiont Proteus mirabilis, induced robust IL-1beta release that was comparable to that induced by the pathogen Salmonella. Upon epithelial injury, production of IL-1beta in the intestine was largely mediated by intestinal Ly6C(high) monocytes, required chemokine receptor CCR2 and was abolished by deletion of IL-1beta in CCR2(+) blood monocytes. Furthermore, colonization with P. mirabilis promoted intestinal inflammation upon intestinal injury via the production of hemolysin, which required NLRP3 and IL-1 receptor signaling in vivo. Thus, upon intestinal injury, selective members of the microbiota stimulate newly recruited monocytes to induce NLRP3-dependent IL-1beta release, which promotes inflammation in the intestine.
Quick Links:
 
Quick Links:
 

Expression

Publication --> Expression annotations

 

Other

19 Bio Entities

0 Expression