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

Sang-Uk Seo, Peter Kuffa, Sho Kitamoto, Hiroko Nagao-Kitamoto, Jenna Rousseau, Yun-Gi Kim, Gabriel Núñez and Nobuhiko Kamada ()
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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

Nature Communications, 2015, vol. 6, issue 1, 1-12

Abstract: 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.

Date: 2015
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DOI: 10.1038/ncomms9010

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