[Research progress on macrophage in radiation induced lung injury]
Mengyao Li1, Pan Liu1, Yuehai Ke1
1School of Basic Medical Sciences, Zhejiang University, Hangzhou 310058, China.
Abstract:
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.
Insights
Radiation-induced lung injury (RILI) involves M1 macrophages causing inflammation and M2 macrophages promoting fibrosis. Understanding macrophage roles offers potential clinical applications for treating lung damage after radiation therapy.
Area of Science:
- Pulmonology
- Immunology
- Oncology
Background:
- Radiation-induced lung injury (RILI) is a common side effect of thoracic radiotherapy.
- Pulmonary macrophages are critical immune cells involved in lung homeostasis and disease.
- RILI encompasses acute radiation pneumonitis and chronic radiation-induced pulmonary fibrosis (RIPF).
Purpose of the Study:
- To review the multifaceted roles of pulmonary macrophages in the pathogenesis of RILI.
- To explore the distinct functions of M1 and M2 macrophages in different stages of RILI.
- To summarize potential clinical applications targeting macrophages for RILI management.
Main Methods:
- Literature review of studies on radiation-induced lung injury.
- Analysis of macrophage activation states (M1 and M2) in RILI.
- Synthesis of findings on cytokine secretion and reactive oxygen species (ROS) production by macrophages.
Main Results:
- M1 macrophages contribute to early-stage inflammation and tissue damage via proinflammatory cytokines and ROS.
- M2 macrophages drive later-stage RILI by secreting profibrotic cytokines, promoting RIPF.
- Macrophages orchestrate the inflammatory and fibrotic responses in RILI.
Conclusions:
- Pulmonary macrophages are key mediators in the development of RILI.
- Targeting specific macrophage polarization states may offer therapeutic strategies for RILI.
- Further research into macrophage-driven pathways is crucial for clinical intervention.
