Intestinal CD169+ macrophages initiate mucosal inflammation by secreting CCL8 that recruits inflammatory monocytes

Kenichi Asano (), Naomichi Takahashi, Mikiko Ushiki, Misa Monya, Fumiaki Aihara, Erika Kuboki, Shigetaka Moriyama, Mayumi Iida, Hiroshi Kitamura, Chun-Hong Qiu, Takashi Watanabe and Masato Tanaka ()
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Kenichi Asano: Laboratory of Immune regulation, School of Life Science, Tokyo University of Pharmacy and Life Sciences
Naomichi Takahashi: Laboratory of Immune regulation, School of Life Science, Tokyo University of Pharmacy and Life Sciences
Mikiko Ushiki: Laboratory of Immune regulation, School of Life Science, Tokyo University of Pharmacy and Life Sciences
Misa Monya: Laboratory of Immune regulation, School of Life Science, Tokyo University of Pharmacy and Life Sciences
Fumiaki Aihara: Laboratory of Immune regulation, School of Life Science, Tokyo University of Pharmacy and Life Sciences
Erika Kuboki: Laboratory of Immune regulation, School of Life Science, Tokyo University of Pharmacy and Life Sciences
Shigetaka Moriyama: Laboratory of Immune regulation, School of Life Science, Tokyo University of Pharmacy and Life Sciences
Mayumi Iida: Laboratory of Immune regulation, School of Life Science, Tokyo University of Pharmacy and Life Sciences
Hiroshi Kitamura: Laboratory of Veterinary Physiology, School of Veterinary Medicine, Rakuno Gakuen University
Chun-Hong Qiu: Institute of Cell Biology, Shandong University School of Medicine
Takashi Watanabe: Immunogenomics Laboratory, RIKEN Center for Integrated Medical Sciences
Masato Tanaka: Laboratory of Immune regulation, School of Life Science, Tokyo University of Pharmacy and Life Sciences

Nature Communications, 2015, vol. 6, issue 1, 1-14

Abstract: Abstract Lamina propria (LP) macrophages are constantly exposed to commensal bacteria, and are refractory to those antigens in an interleukin (IL)-10-dependent fashion. However, the mechanisms that discriminate hazardous invasion by bacteria from peaceful co-existence with them remain elusive. Here we show that CD169+ macrophages reside not at the villus tip, but at the bottom-end of the LP microenvironment. Following mucosal injury, the CD169+ macrophages recruit inflammatory monocytes by secreting CCL8. Selective depletion of CD169+ macrophages or administration of neutralizing anti-CCL8 antibody ameliorates the symptoms of experimentally induced colitis in mice. Collectively, we identify an LP-resident macrophage subset that links mucosal damage and inflammatory monocyte recruitment. Our results suggest that CD169+ macrophage-derived CCL8 serves as an emergency alert for the collapse of barrier defence, and is a promising target for the suppression of mucosal injury.

Date: 2015
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DOI: 10.1038/ncomms8802

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