A Large Polysaccharide Produced by Helicobacter hepaticus Induces an Anti-inflammatory Gene Signature in Macrophages

Camille Danne (Lead / Corresponding author), Grigory Ryzhakov, Maria Martínez-López, Nicholas Edward Ilott, Fanny Franchini, Fiona Cuskin, Elisabeth C. Lowe, Samuel J. Bullers, J. Simon C. Arthur, Fiona Powrie

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34 Citations (Scopus)
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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.

Original languageEnglish
Pages (from-to)733-745.e5
Number of pages18
JournalCell Host & Microbe
Issue number6
Early online date13 Dec 2017
Publication statusPublished - 13 Dec 2017


  • Journal article
  • Inflammatory bowel disease
  • Host-microbe interactions
  • Mutualism
  • Helicobacter hepaticus
  • Macrophage
  • Anti-inflammatory gene signature
  • Polysaccharide
  • TLR2
  • CREB
  • MSK1/2

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