@article{oai:rakuno.repo.nii.ac.jp:00002267,
 author = {Asano, Kenichi and Takahashi, Naomichi and Ushiki, Mikiko and Monya, Misa and Aihara, Fumiaki and Kuboki, Erika and Moriyama, Shigetaka and Iida, Mayumi and Kitamura, Hiroshi and Qiu, Chun-Hong and Watanabe, Takashi and Tanaka, Masato},
 journal = {Nature Communications},
 month = {Jul},
 note = {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.},
 pages = {7802-1--7802-14},
 title = {Intestinal CD169^+ macrophages initiate mucosal inflammation by secreting CCL8 that recruits inflammatory monocytes},
 volume = {6},
 year = {2015}
}