Journal
IMMUNOPHARMACOLOGY AND IMMUNOTOXICOLOGY
Volume 41, Issue 3, Pages 370-379Publisher
TAYLOR & FRANCIS LTD
DOI: 10.1080/08923973.2018.1533025
Keywords
Radiation; fibrosis; macrophages; PPAR
Categories
Funding
- Science and Engineering Research Board, Department of Science and Technology, Government of India [YSS/2014/000518/LS]
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Lung cancer continues to be the leading cause of cancer deaths and more than one million lung cancer patients will die every year worldwide. Radiotherapy (RT) plays an important role in lung cancer treatment, but the side effects of RT are pneumonitis and pulmonary fibrosis. RT-induced lung injury causes damage to alveolar-epithelial cells and vascular endothelial cells. Macrophages play an important role in the development of pulmonary fibrosis despite its role in immune response. These injury activated macrophages develop into classically activated M1 macrophage or alternative activated M2 macrophage. It secretes cytokines, interleukins, interferons, and nitric oxide. Several pro-inflammatory lipids and pro-apoptotic proteins cause lipotoxicity such as LDL, FC, DAG, and FFA. The overall findings in this review conclude the importance of macrophages in inducing toxic/inflammatory effects during RT of lung cancer, which is clinically vital to treat the radiation-induced fibrosis.
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