Journal
CELL HOST & MICROBE
Volume 22, Issue 6, Pages 733-+Publisher
CELL PRESS
DOI: 10.1016/j.chom.2017.11.002
Keywords
-
Categories
Funding
- Cancer Research UK [OCRC-DPhil13-FF]
- Kennedy Trust [KENN 15 16 03]
- Spanish Ministry of Education, Culture, and Sport
- Wellcome Trust UK [095688/Z/11/Z]
- ERC grant [Ares(2013)3687660]
- Fondation Louis Jeantet
Ask authors/readers for more resources
Interactions between the host and its microbiota are of mutual benefit and promote health. Complex molecular pathways underlie this dialog, but the identity of microbe-derived molecules that mediate the mutualistic state remains elusive. Helicobacter hepaticus is a member of the mouse intestinal microbiota that is tolerated by the host. In the absence of an intact IL-10 signaling, H. hepaticus induces an IL-23-driven inflammatory response in the intestine. Here we investigate the interactions between H. hepaticus and host immune cells that may promote mutualism, and the microbe-derived molecule(s) involved. Our results show that H. hepaticus triggers early IL-10 induction in intestinal macrophages and produces a large soluble polysaccharide that activates a specific MSK/CREB-dependent antiinflammatory and repair gene signature via the receptor TLR2. These data identify a host-bacterial interaction that promotes mutualistic mechanisms at the intestinal interface. Further understanding of this pathway may provide novel prevention and treatment strategies for inflammatory bowel disease.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available