Intestinal CD169^+ macrophages initiate mucosal inflammation by secreting CCL8 that recruits inflammatory monocytes
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Article
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.
収録刊行物
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- Nature Communications
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Nature Communications 6 7802-1-7802-14, 2015-07
Macmillan Publishers Limited
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詳細情報 詳細情報について
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- CRID
- 1050564287442047104
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- NII論文ID
- 120006311913
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- HANDLE
- 10659/4987
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- 本文言語コード
- en
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- 資料種別
- journal article
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- データソース種別
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- IRDB
- CiNii Articles