高原肺水肿中的炎症与巨噬细胞免疫作用

Inflammation and Macrophage Immunity in High Altitude Pulmonary Edema

高原肺水肿(High Altitude Pulmonary Edema, HAPE)是机体对低氧环境不同程度适应性导致肺液稳态调节不平衡而引起的高原危重症。目前已有的发生机制主要为血流动力学、渗液机制、肺水清除障碍、炎症反应等。缺氧诱导的炎症机制参与了HAPE,肺泡和肺血管壁中最突出的炎症细胞类型是巨噬细胞。本研究拟通过综述类形式从炎症与巨噬细胞免疫作用角度谈HAPE的发病机制及研究进展,以期对HAPE的研究及临床预防和(或)治疗具有一定推动作用。

High Altitude Pulmonary Edema (HAPE) is a critical illness caused by imbalance of lung fluid ho-meostasis regulation due to different degrees of adaptation to low oxygen environment. Currently, the main mechanisms of HAPE are hemodynamics, exudate mechanism, impaired lung water clear-ance, and inflammatory response. Hypoxia-induced inflammatory mechanisms are involved in HAPE, and the most prominent inflammatory cell type in the alveolar and pulmonary vascular walls are macrophages. This study intends to discuss the pathogenesis and research progress of HAPE from the perspective of inflammation and macrophage immune action in the form of a review class, in order to have a promotion effect on the research and clinical prevention and/or treatment of HAPE.