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）是肺癌、食管癌等恶性肿瘤患者进行放射治疗时产生的不良反应，包括急性放射性肺炎和慢性放射性肺纤维化。肺巨噬细胞是维持肺部稳态的一种天然免疫细胞，在RILI整个病理过程中均发挥关键作用。在RILI早期，肺巨噬细胞发生M1型活化，分泌炎性细胞因子，诱导炎症反应，同时通过促进活性氧诱导的活性氧级联反应产生大量活性氧，进一步损伤肺组织。在RILI中晚期，肺巨噬细胞向M2型转化，分泌促纤维细胞因子，促进放射性肺纤维化的发展。本文总结了肺巨噬细胞在RILI发病机制中的作用以及潜在的临床应用前景。
Keywords: Inflammation; Macrophages; Pulmonary fibrosis; Radiation-induced lung injury; Reactive oxygen species; Review.