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Intestinal macrophages arising from CCR2+ monocytes control pathogen infection by activating innate lymphoid cells

Author

Listed:
  • Sang-Uk Seo

    (University of Michigan Medical School)

  • Peter Kuffa

    (University of Michigan Medical School)

  • Sho Kitamoto

    (University of Michigan Medical School)

  • Hiroko Nagao-Kitamoto

    (University of Michigan Medical School)

  • Jenna Rousseau

    (University of Michigan Medical School)

  • Yun-Gi Kim

    (University of Michigan Medical School)

  • Gabriel Núñez

    (University of Michigan Medical School)

  • Nobuhiko Kamada

    (University of Michigan Medical School)

Abstract

Monocytes play a crucial role in antimicrobial host defence, but the mechanisms by which they protect the host during intestinal infection remains poorly understood. Here we show that depletion of CCR2+ monocytes results in impaired clearance of the intestinal pathogen Citrobacter rodentium. After infection, the de novo recruited CCR2+ monocytes give rise to CD11c+CD11b+F4/80+CD103− intestinal macrophages (MPs) within the lamina propria. Unlike resident intestinal MPs, de novo differentiated MPs are phenotypically pro-inflammatory and produce robust amounts of IL-1β (interleukin-1β) through the non-canonical caspase-11 inflammasome. Intestinal MPs from infected mice elicit the activation of RORγt+ group 3 innate lymphoid cells (ILC3) in an IL-1β-dependent manner. Deletion of IL-1β in blood monocytes blunts the production of IL-22 by ILC3 and increases the susceptibility to infection. Collectively, these studies highlight a critical role of de novo differentiated monocyte-derived intestinal MPs in ILC3-mediated host defence against intestinal infection.

Suggested Citation

  • Sang-Uk Seo & Peter Kuffa & Sho Kitamoto & Hiroko Nagao-Kitamoto & Jenna Rousseau & Yun-Gi Kim & Gabriel Núñez & Nobuhiko Kamada, 2015. "Intestinal macrophages arising from CCR2+ monocytes control pathogen infection by activating innate lymphoid cells," Nature Communications, Nature, vol. 6(1), pages 1-12, November.
    • Handle: RePEc:nat:natcom:v:6:y:2015:i:1:d:10.1038_ncomms9010
    DOI: 10.1038/ncomms9010
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