@article{oai:repo.qst.go.jp:00045243,
 author = {Sakai, Minako and Iwakawa, Mayumi and Iwakura, Youichirou and Oota, Toshie and Tsujii, Hirohiko and Imai, Takashi and 酒井 美奈子 and 岩川 眞由美 and 太田 敏江 and 辻井 博彦 and 今井 高志},
 issue = {4},
 journal = {Journal of Radiation Research},
 month = {Jul},
 note = {To understand the molecular mechanisms that underlie radiation pneumonitis, we examined whether knockout of the TNF or the IL-6 gene could give mice an inherent resistance to radiation in the acute phase of alveolar damage after thoracic irradiation. The temporal expression of inflammation (CD44) and apoptosis (Bak) markers in lung after thoracic irradiation was measured to determine the degree of alveolar damage. At 4 weeks post-irradiation (10 Gy), small inflammatory foci were observed in all mice, but there were no obvious histological differences between control (C57BL/6JSlc), TNF-alpha knockout (TNF KO), and IL-6 knockout (IL-6 KO) mice. However, immunohistochemical analysis of CD44 and Bak expression over a time course of 2 weeks highlighted significant differences between the three groups. C57BL/6JSlc and TNF KO mice had increased numbers of both CD44-positive and Bak-positive cells after irradiation, while the IL-6 KO mice showed stable levels of CD44 and Bak. In conclusion, the radioresistant status of IL-6 KO mice in the acute phase of alveolar damage after irradiation suggested an important role for IL-6 in radiation pneumonitis.},
 pages = {409--416},
 title = {CD44 and Bak expression in IL-6 or TNF-alpha gene knockout mice after whole lung irradiation},
 volume = {49},
 year = {2008}
}