Radiation-induced lung injury

About: Radiation-induced lung injury is a research topic. Over the lifetime, 258 publications have been published within this topic receiving 6877 citations. The topic is also known as: Radiation Pneumonitis.

Molecular and cellular mediators in radiation-induced lung injury

Abstract: Xuebin Yang: Molecular and Cellular Mediators In Radiation-Induced Lung Injury (Under the direction of Suzanne Kirby, M.D. Ph.D) Radiation-induced lung injury is a common adverse effect in patients receiving thoracic irradiation and for which, there is currently no effective therapy. Using a murine model of thoracic irradiation, we found that mice deficient in either the chemokine CCL3 or one of its receptors, CCR1, are significantly protected from radiation lung injury. This protected phenotype includes improved survival, virtually no pneumonitis or fibrosis, and preserved lung function when compared to wild-type mice. We further showed that a specific CCR1 inhibitor, BX471 provided similar protection. Therefore, CCR1 is a promising target for reducing radiation lung injury. To investigate the mechanisms by which CCL3/CCR1 signalling mediates radiation lung injury, we evaluated their influence on lung inflammation after irradiation. When compared with irradiated WT mice, irradiated CCL3and CCR1-deficient mice had less lung infiltration of CD4 + and CD8 + T cells; however, CD4-deficient mice showed only partial protection, while CD8-deficient mice had slightly worse fibrosis. We further analyzed inflammatory cytokines and different subsets of CD4 + lymphocytes, T H 1, T H 2, T H 17 and Treg cells, in our model. We found no differences in lung Foxp3 + Treg cells between WT and CCR1-deficient mice. Notably however, irradiated CCR1-deficient mice had less mRNA

Evaluation of the relationship between the range of radiation-induced lung injury on CT images after IMRT for stage I lung cancer and dosimetric parameters.

Abstract: This study evaluated the correlation between radiation-induced lung injury (RILI) and dosimetric parameters on computed tomography (CT) images of stage I non-small cell lung cancer (NSCLC) patients...

Preventive and Therapeutic Effect of Aidi Injection on Radiation-Induced Lung Injury

Abstract: Objective To study the effect of aidi injection on radiation-induced lung injury and the probable Mechanism. Methods One hundred and twenty C57BL /6 mice were exposed to either sham radiation or single fraction of 12 Gy delivered to the thorax. Four groups were defined as follows: in normal control group,the mice received neither radiation nor drug; in aidi injection + radiation group,the mice received radiation and aidi injection; in Solu Medrol + radiation group,the mice received Solu Medrol; in radiation group,the mice were exposed to radiation. Aidi or Solu Medrol were injected intraperitoneally 2 h before the radiation and daily after the radiation. Mice were sacrificed 1,24,72 hours,1,2,4,8,16 and 24 weeks after radiation. The left lungs were fixed and sectioned. The sections were stained by haematoxylin and eosin,masson stain and immunohistochemical stain for transforming growth factor β1( TGF-β1). The right lungs were collected to detect TGF-β1mRNA expression by real-time quantitative reverse transcipiase polymerase chain reaction( RT-PCR) and TGF-β1protein expression by Western blotting. Results Pneumonitis developed 1 to 2 weeks after radiation. Their TGF-β1mRNA and protein expression levels in radiation-treated mice were significantly higher than those in normal control group( both P 0. 05). But the effects were reversed by aidi and Solu Medrol treatment( P 0. 05). The TGF-β1mRNA and protein expression levels were not significantly different between aidi and Solu Medrol treatment. Conclusion Both aidi injection and Solu Medrol can significantly downregulate TGF-β1mRNA and protein expression levels in the lungs of mice with radiation-induced lung injury. There is no significant difference in the effect between aidi injection and Solu Medrol.