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

Research output: Contribution to journalArticlepeer-review

28 Citations (Scopus)
232 Downloads (Pure)

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.

Original languageEnglish
Pages (from-to)733-745.e5
Number of pages18
JournalCell Host & Microbe
Volume22
Issue number6
Early online date13 Dec 2017
DOIs
Publication statusPublished - 13 Dec 2017

Keywords

  • 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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