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


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2015-12

AUTHORS

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

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. More... »

PAGES

8010

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/ncomms9010

    DOI

    http://dx.doi.org/10.1038/ncomms9010

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1042722101

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/26269452


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