2024-03-29T15:23:42Zhttp://repisalud.isciii.es/oai/requestoai:repisalud.isciii.es:20.500.12105/73102023-10-09T14:36:27Zcom_20.500.12105_2145com_20.500.12105_2051com_20.500.12105_2144col_20.500.12105_2146
00925njm 22002777a 4500
dc
Danne, Camille
author
Ryzhakov, Grigory
author
Martinez-Lopez, Maria
author
Ilott, Nicholas Edward
author
Franchini, Fanny
author
Cuskin, Fiona
author
Lowe, Elisabeth C
author
Bullers, Samuel J
author
Arthur, J Simon C
author
Powrie, Fiona
author
2017-12-13
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.
Cell Host Microbe. 2017; 22(6):733-745
1931-3128
http://hdl.handle.net/20.500.12105/7310
29241040
10.1016/j.chom.2017.11.002
1934-6069
Cell host & microbe
CREB
Helicobacter hepaticus
MSK1/2
TLR2
Anti-inflammatory gene signature
Host-microbe interactions
Inflammatory bowel disease
Macrophage
Mutualism
Polysaccharide
A Large Polysaccharide Produced by Helicobacter hepaticus Induces an Anti-inflammatory Gene Signature in Macrophages