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Spleen-derived classical monocytes mediate lung ischemia-reperfusion injury through IL-1β.


ABSTRACT: Ischemia-reperfusion injury, a form of sterile inflammation, is the leading risk factor for both short-term mortality following pulmonary transplantation and chronic lung allograft dysfunction. While it is well recognized that neutrophils are critical mediators of acute lung injury, processes that guide their entry into pulmonary tissue are not well understood. Here, we found that CCR2+ classical monocytes are necessary and sufficient for mediating extravasation of neutrophils into pulmonary tissue during ischemia-reperfusion injury following hilar clamping or lung transplantation. The classical monocytes were mobilized from the host spleen, and splenectomy attenuated the recruitment of classical monocytes as well as the entry of neutrophils into injured lung tissue, which was associated w

SUBMITTER: Hsiao HM 

PROVIDER: S-EPMC6025976 | biostudies-literature | 2018 Jul

REPOSITORIES: biostudies-literature

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