TY-JUR T1 - 稳态和早期募集的CD101 ^{- 嗜酸性粒细胞抑制内毒素诱导的急性肺损伤JF - 欧洲呼吸期刊Jo - EUR RESPIR J DO - 10.1183 / 13993003.02354-2019 VL - 56是 - 5SP - 1902354 Au - zhu，陈奥 - 翁，青玉奥 - 周，凌任奥 - 曹，潮奥 - 李，费奥乌 - 吴，尹芳坝，延平奥李，苗奥 - 胡，岳奥申，嘉新奥 - 熊，薛芳，兰，芬芳，李霞，李霞奥 - 张，宾·奥 - 张，郝·黄，人互惠ying，宋闽奥申，华浩奥 - 陈，志华·李，文y1 - 2020/11/01 ur - //www.qdcxjkg.com/content/56/5/1902354。摘要N2 - 引入急性肺损伤（ALI）是一种致命但下降的病症，具有严重的中性炎症炎症，尽管关于嗜酸性粒细胞在Ali发病机制中的功能毫无熟悉。我们的目标是探讨Ali中嗜酸性粒细胞的作用和分子机制。方法通过流式细胞术鉴定了肺嗜酸性粒细胞。使用具有丰富或缺乏嗜酸性粒细胞的小鼠。确定了嗜酸性粒细胞和中性粒细胞在支气管肺泡灌洗液，炎症评估和存活率中的细胞性。人类样品也用于验证实验结果。患有急性呼吸窘迫综合征（ARDS）的存活患者，血液嗜酸性血液粒细胞均与皮质类固醇用途无关。在小鼠中存在肺实质嗜酸性嗜酸性粒细胞，这些稳态粒细胞源于骨髓，主要是CD101-。可以比脂多糖（LPS） - intiated嗜嗜益症炎前招募更多CD101-嗜酸性粒细胞。 Loss of eosinophils augmented LPS-induced pulmonary injury. Homeostatic CD101− eosinophils ameliorated, while allergic CD101+ eosinophils exacerbated, the neutrophilic inflammation induced by LPS. Likewise, CD101 expression in eosinophils from ARDS patients did not differ from healthy subjects. Mechanistically, CD101− eosinophils exhibited higher levels of Alox15 and Protectin D1. Administration of Protectin D1 isomer attenuated the neutrophilic inflammation.Conclusions Collectively, our findings identify an uncovered function of native CD101− eosinophils in suppressing neutrophilic lung inflammation and suggest a potential therapeutic target for ALI.Eosinophils, a type of immune cell easily overlooked in nonallergic inflammatory diseases, could reside and be rapidly recruited into lungs to suppress endotoxin-induced acute lung injury https://bit.ly/3dyvCaD ER -}