Li Mengyao, Liu Pan, Ke Yuehai, Zhang Xue
School of Basic Medical Sciences, Zhejiang University, Hangzhou 310058, China.
Zhejiang Da Xue Xue Bao Yi Xue Ban. 2020 Oct 25;49(5):623-628. doi: 10.3785/j.issn.1008-9292.2020.10.12.
Radiation-induced lung injury (RILI), including acute radiation pneumonitis and chronic radiation-induced pulmonary fibrosis (RIPF), is a side effect of radiotherapy for lung cancer and esophageal cancer. Pulmonary macrophages, as a kind of natural immune cells maintaining lung homeostasis, play a key role in the whole pathological process of RILI. In the early stage of RILI, classically activated M1 macrophages secrete proinflammatory cytokines to induce inflammation and produce massive reactive oxygen species (ROS) through ROS-induced cascade to further impair lung tissue. In the later stage of RILI, alternatively activated M2 macrophages secrete profibrotic cytokines to promote the development of RIPF. The roles of macrophage in the pathogenesis of RILI and the related potential clinical applications are summarized in this review.
放射性肺损伤（RILI），包括急性放射性肺炎和慢性放射性肺纤维化（RIPF），是肺癌和食管癌放射治疗的一种副作用。肺巨噬细胞作为维持肺稳态的一种天然免疫细胞，在RILI的整个病理过程中起关键作用。在RILI的早期，经典激活的M1巨噬细胞分泌促炎细胞因子以诱导炎症，并通过ROS诱导的级联反应产生大量活性氧（ROS），从而进一步损害肺组织。在RILI的后期，交替激活的M2巨噬细胞分泌促纤维化细胞因子以促进RIPF的发展。本文综述了巨噬细胞在RILI发病机制中的作用及相关潜在临床应用。
