Please use this identifier to cite or link to this item:http://hdl.handle.net/20.500.12105/7310
A Large Polysaccharide Produced by Helicobacter hepaticus Induces an Anti-inflammatory Gene Signature in Macrophages
Cell Host Microbe. 2017; 22(6):733-745
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 anti-inflammatory 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.
CREB | Helicobacter hepaticus | MSK1/2 | TLR2 | anti-inflammatory gene signature | host-microbe interactions | inflammatory bowel disease | macrophage | mutualism | polysaccharide
Animals | Helicobacter hepaticus | Immunosuppressive Agents | Interleukin-10 | Interleukin-23 | Macrophages | Mice | Polysaccharides, Bacterial | Toll-Like Receptor 2 | Symbiosis