IL-10-producing intestinal macrophages prevent excessive antibacterial innate immunity by limiting IL-23 synthesis

Petra Krause, Venetia Morris, Jason A. Greenbaum, Yoon Park, Unni Bjoerheden, Zbigniew Mikulski, Tracy Muffley, Jr-Wen Shui, Gisen Kim, Hilde Cheroutre, Yun-Cai Liu, Bjoern Peters, Mitchell Kronenberg () and Masako Murai ()
Additional contact information
Petra Krause: La Jolla Institute for Allergy and Immunology
Venetia Morris: La Jolla Institute for Allergy and Immunology
Jason A. Greenbaum: Bioinformatics Core Facility, La Jolla Institute for Allergy and Immunology
Yoon Park: La Jolla Institute for Allergy and Immunology
Unni Bjoerheden: La Jolla Institute for Allergy and Immunology
Zbigniew Mikulski: Microscopy Core Facility, La Jolla Institute for Allergy and Immunology
Tracy Muffley: La Jolla Institute for Allergy and Immunology
Jr-Wen Shui: La Jolla Institute for Allergy and Immunology
Gisen Kim: La Jolla Institute for Allergy and Immunology
Hilde Cheroutre: La Jolla Institute for Allergy and Immunology
Yun-Cai Liu: La Jolla Institute for Allergy and Immunology
Bjoern Peters: La Jolla Institute for Allergy and Immunology
Mitchell Kronenberg: La Jolla Institute for Allergy and Immunology
Masako Murai: La Jolla Institute for Allergy and Immunology

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

Abstract: Abstract Innate immune responses are regulated in the intestine to prevent excessive inflammation. Here we show that a subset of mouse colonic macrophages constitutively produce the anti-inflammatory cytokine IL-10. In mice infected with Citrobacter rodentium, a model for enteropathogenic Escherichia coli infection in humans, these macrophages are required to prevent intestinal pathology. IL-23 is significantly increased in infected mice with a myeloid cell-specific deletion of IL-10, and the addition of IL-10 reduces IL-23 production by intestinal macrophages. Furthermore, blockade of IL-23 leads to reduced mortality in the context of macrophage IL-10 deficiency. Transcriptome and other analyses indicate that IL-10-expressing macrophages receive an autocrine IL-10 signal. Interestingly, only transfer of the IL-10 positive macrophages could rescue IL-10-deficient infected mice. Therefore, these data indicate a pivotal role for intestinal macrophages that constitutively produce IL-10, in controlling excessive innate immune activation and preventing tissue damage after an acute bacterial infection.

Date: 2015
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DOI: 10.1038/ncomms8055

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