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                  <mods:namePart>Foundation Lous Jeantet</mods:namePart>
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               <mods:name>
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                  <mods:namePart>Unión Europea. Comisión Europea</mods:namePart>
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               <mods:name>
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                  <mods:namePart>Unión Europea. Comisión Europea. European Research Council (ERC)</mods:namePart>
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               <mods:identifier type="citation">Cell Host Microbe. 2017; 22(6):733-745</mods:identifier>
               <mods:identifier type="doi">10.1016/j.chom.2017.11.002</mods:identifier>
               <mods:identifier type="e-issn">1934-6069</mods:identifier>
               <mods:identifier type="issn">1931-3128</mods:identifier>
               <mods:identifier type="journal">Cell host &amp; microbe</mods:identifier>
               <mods:identifier type="pubmedID">29241040</mods:identifier>
               <mods:identifier type="uri">http://hdl.handle.net/20.500.12105/7310</mods:identifier>
               <mods:abstract>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.</mods:abstract>
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                  <mods:topic>CREB</mods:topic>
               </mods:subject>
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                  <mods:topic>Helicobacter hepaticus</mods:topic>
               </mods:subject>
               <mods:subject>
                  <mods:topic>MSK1/2</mods:topic>
               </mods:subject>
               <mods:subject>
                  <mods:topic>TLR2</mods:topic>
               </mods:subject>
               <mods:subject>
                  <mods:topic>Anti-inflammatory gene signature</mods:topic>
               </mods:subject>
               <mods:subject>
                  <mods:topic>Host-microbe interactions</mods:topic>
               </mods:subject>
               <mods:subject>
                  <mods:topic>Inflammatory bowel disease</mods:topic>
               </mods:subject>
               <mods:subject>
                  <mods:topic>Macrophage</mods:topic>
               </mods:subject>
               <mods:subject>
                  <mods:topic>Mutualism</mods:topic>
               </mods:subject>
               <mods:subject>
                  <mods:topic>Polysaccharide</mods:topic>
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                  <mods:title>A Large Polysaccharide Produced by Helicobacter hepaticus Induces an Anti-inflammatory Gene Signature in Macrophages</mods:title>
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