中性粒细胞胞外陷阱
生物
卡氏肺孢子虫
肺孢子虫肺炎
免疫学
体内
发病机制
白三烯B4
微生物学
耶氏肺孢子虫
炎症
人类免疫缺陷病毒(HIV)
生物技术
作者
Yanxi Zhou,Shuwei Deng,Chunjing Du,Liang Zhang,Li Lan,Yujia Liu,Yijie Wang,Yue Zhang,Liuluan Zhu
标识
DOI:10.1002/eji.202350779
摘要
Abstract Pneumocystis pneumonia (PCP) is a fungal pulmonary disease with high mortality in immunocompromised patients. Neutrophils are essential in defending against fungal infections; however, their role in PCP is controversial. Here we aim to investigate the effects of neutrophil extracellular traps (NETs) on Pneumocystis clearance and lung injury using a mouse model of PCP. Intriguingly, although neutrophils play a fundamental role in defending against fungal infections, NETs failed to eliminate Pneumocystis , but instead impaired the killing of Pneumocystis . Mechanically, Pneumocystis triggered Leukotriene B4 (LTB4)‐dependent neutrophil swarming, leading to agglutinative NET formation. Blocking Leukotriene B4 with its receptor antagonist Etalocib significantly reduced the accumulation and NET release of neutrophils in vitro and in vivo , enhanced the killing ability of neutrophils against Pneumocystis , and alleviated lung injury in PCP mice. This study identifies the deleterious role of agglutinative NETs in Pneumocystis infection and reveals a new way to prevent NET formation, which provides new insights into the pathogenesis of PCP.
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