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oai:repisalud.isciii.es:20.500.12105/73102024-09-27T09:06:42Zcom_20.500.12105_19604com_20.500.12105_2051col_20.500.12105_19605

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 10.1016/j.chom.2017.11.002 1934-6069 1931-3128 Cell host & microbe 29241040 http://hdl.handle.net/20.500.12105/7310 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