急性呼吸窘迫综合征
炎症
弥漫性肺泡损伤
肺泡巨噬细胞
肺
免疫学
免疫系统
医学
分泌物
巨噬细胞
生物
急性呼吸窘迫
内科学
体外
生物化学
作者
Huan Tao,Younian Xu,Shihai Zhang
出处
期刊:Inflammation
[Springer Nature]
日期:2022-09-01
卷期号:46 (1): 47-55
被引量:55
标识
DOI:10.1007/s10753-022-01726-w
摘要
Acute lung injury (ALI) usually causes acute respiratory distress syndrome (ARDS), or even death in critical ill patients. Immune cell infiltration in inflamed lungs is an important hallmark of ARDS. Macrophages are a type of immune cell that participate in the entire pathogenic trajectory of ARDS and most prominently via their interactions with lung alveolar epithelial cells (AECs). In the early stage of ARDS, classically activated macrophages secrete pro-inflammatory cytokines to clearance of the pathogens which may damage alveolar AECs cell structure and result in cell death. Paradoxically, in late stage of ARDS, anti-inflammatory cytokines secreted by alternatively activated macrophages dampen the inflammation response and promote epithelial regeneration and alveolar structure remodeling. In this review, we discuss the important role of macrophages and AECs in the progression of ARDS.
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