PT -期刊文章盟朱、陈盟-翁,胡庆余堂盟——周Ling-Ren盟——曹、曹AU -李,范盟——吴Yin-Fang盟——吴,严萍AU -李,苗族非盟-胡,越盟——沈Jia-Xin盟——熊,徐方AU - Lan,分盟,夏Li-Xia盟——张,本盟——张郝盟——黄,人非盟-应Song-Min盟——沈Hua-Hao盟——陈志华AU - Li，温家宝TI -稳态和early-recruited CD101 <一口>−< / >共舞,嗜酸性粒细胞抑制endotoxin-induced急性肺损伤援助- 10.1183/13993003.02354 -2019 DP - 2020年11月01 TA -欧洲呼吸杂志》第六PG - 1902354 - 56 IP - 4100 4099 - //www.qdcxjkg.com/content/56/5/1902354.short //www.qdcxjkg.com/content/56/5/1902354.fullSO - Eur Respir J2020 Nov 01;急性肺损伤(ALI)是一种致命但治疗不足的严重中性粒细胞性炎症，尽管对嗜酸性粒细胞在ALI发病机制中的功能知之甚少。我们的目的是研究嗜酸性粒细胞在ALI中的作用和分子机制。方法采用流式细胞仪检测肺嗜酸性粒细胞。使用嗜酸性粒细胞充足或不足的小鼠。测定支气管肺泡灌洗液中嗜酸性粒细胞和中性粒细胞的细胞数量、炎症评估和生存率。人体样本也用于验证实验结果。结果急性呼吸窘迫综合征(ARDS)患者外周血嗜酸性粒细胞增多，与激素使用无关。 There existed homeostatic eosinophils in lung parenchyma in mice and these homeostatic eosinophils, originating from the bone marrow, were predominantly CD101−. More CD101− eosinophils could be recruited earlier than lipopolysaccharide (LPS)-initiated neutrophilic inflammation. 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