@article{oai:repo.qst.go.jp:00046162,
 author = {Saito-Fujita, Tomoko and Iwakawa, Mayumi and Nakamura, Etsuko and Nakawatari, Miyako and Fujita, Hidetoshi and Moritake, Takashi and Imai, Takashi and 藤田 知子 and 岩川 眞由美 and 中村 悦子 and 中渡 美也子 and 藤田 英俊 and 盛武 敬 and 今井 高志},
 issue = {3},
 journal = {Journal of Radiation Research},
 month = {May},
 note = {There is a great deal of evidence that a cyclic cascade of inflammatory cytokines, together with the activation of macrophages, is initiated very early after irradiation to develop lung fibrosis in a late phase. To understand the persistent effects of cytokines, the cytokine gene of knock out or transgenic mouse is one of the useful tools. In this study, we evaluated a role of a key molecule, interleukin-6 (IL-6), in the late-phase inflammatory response and subsequent fibrotic changes after irradiation using wild-type (WT) and IL-6 knock out (IL-6 KO) mice. The mice underwent thoracic irradiation with 10 Gy of C-ion beam or sham-irradiation and were examined by histology. Immunoreactivity for IL-6 was induced at the site of bronchiolar epithelium, in pneumocytes and in monocytes by C-ion irradiation. At 24 weeks after irradiation, the infiltration of macrophages, detected by positive immunohistological staining with Mac3 antibody, was observed in alveolar spaces both in WT and IL-6 KO mice. The thickening of bronchiolar and alveolar walls exhibited in WT mice, but not KO mice, and fibrotic changes detected by Masson-Trichrome staining, were observed only in the lungs of WT mice, while it was attenuated in IL-6 KO mice. These results indicated that IL-6 might not be essential for activating macrophages in the late phase, but plays an important role for fibrotic changes of the alveolar wall after irradiation.},
 pages = {270--277},
 title = {Attenuated Lung Fibrosis in Interleukin 6 Knock-out Mice after C-ion Irradiation to Lung},
 volume = {52},
 year = {2011}
}