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Nat Commun. 2015 Jul 21;6:7802. doi: 10.1038/ncomms8802.

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

Author information

1
1] Laboratory of Immune regulation, School of Life Science, Tokyo University of Pharmacy and Life Sciences, 1432-1 Horinouchi, Hachioji, Tokyo 192-0392, Japan [2] Japan Science and Technology Agency, PRESTO, 4-1-8 Honcho, Kawaguchi, Saitama 332-0012, Japan.
2
Laboratory of Immune regulation, School of Life Science, Tokyo University of Pharmacy and Life Sciences, 1432-1 Horinouchi, Hachioji, Tokyo 192-0392, Japan.
3
Laboratory of Veterinary Physiology, School of Veterinary Medicine, Rakuno Gakuen University, 582 Bunkyodai-Midorimachi, Ebetsu, Hokkaido 069-8501, Japan.
4
Institute of Cell Biology, Shandong University School of Medicine, PO Box 73, No. 44 Wenhua Xi Road, Jinan, Shandong 250012, China.
5
Immunogenomics Laboratory, RIKEN Center for Integrated Medical Sciences, 1-7-22 Suehirocho, Tsurumi, Yokohama 227-0045, Japan.

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.

PMID:
26193821
PMCID:
PMC4518321
DOI:
10.1038/ncomms8802
[Indexed for MEDLINE]
Free PMC Article

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