Cytokine, chemokine alterations and immune cell infiltration in Radiation-induced lung injury: Implications for prevention and management

Radiation therapy is one of the primary treatments for thoracic malignancies, with radiation-induced lung injury (RILI) emerging as its most prevalent complication. RILI encompasses early-stage radiation pneumonitis (RP) and the subsequent development of radiation pulmonary fibrosis (RPF). During radiation treatment, not only are tumor cells targeted, but normal tissue cells, including alveolar epithelial cells and vascular endothelial cells, also sustain damage. Within the lungs, ionizing radiation boosts the intracellular levels of reactive oxygen species across various cell types. This elevation precipitates the release of cytokines and chemokines, coupled with the infiltration of inflammatory cells, culminating in the onset of RP. This pulmonary inflammatory response can persist, spanning a duration from several months to years, ultimately progressing to RPF. This review aims to explore the alterations in cytokine and chemokine release and the influx of immune cells post-ionizing radiation exposure in the lungs, offering insights for the prevention and management of RILI.

Automated summary

Radiation therapy is an effective treatment for thoracic malignancies, but it can cause radiation-induced lung injury (RILI), including radiation pneumonitis (RP) and radiation pulmonary fibrosis (RPF). The damage to normal lung cells during radiation treatment leads to a pulmonary inflammatory response, resulting in RP and RPF.