1）IL-17欠損マウスでブレオマイシン誘発急性肺損傷が増悪する機序を検討し、IL-12発現樹状細胞の関与が推測された。2）高濃度酸素曝露による内皮細胞反応性亢進に伴い、パターン認識受容体TLR family、NOD family遺伝子発現の変動を認めた。3）ヒトES細胞の空気接触環境下における肺胞上皮細胞への分化を、SPC、aquaporin-5(AP5)をマーカーとして検討し、SPC発現は培養20日後に増加、40日後には減少、AP5発現は時間とともに増加した。4）ヒトのARDS、IPF剖検肺で、肺組織幹細胞・前駆細胞を探索するも確認できなかった。
1) We examined the mechanisms of exaggerated bleomycin-induced acute lung injury in IL-17-deficient mice, and found that IL-12-expressing dendritic cells were increased in the knockout mice. 2) In human endothelial cells, in association with the accelerated response, gene expression of TLR and NOD families were significantly affected under hyperoxia. 3) We examined the differentiation of human embryonic stem cells to alveolar epithelial cells under air-liquid interface, using SPC and AP5 as markers. The expression of SPC was increased at 20 days, but was decreased at 40 days, whereas that of AP5 was increased with time. 4) We examined lung stem cells and progenitor cells in autopsied lungs from patients with ARDS and IPF. In ARDS, accumulation of inflammatory cells in the early phase and metaplastic epithelial cells in the late phase were observed, but Musashi-1 and SPC double positive cells were not observed. In IPF, Musashi-1 and CCSP double positive cells were also not observed.

研究種目 : 基盤研究(C)
研究期間 : 2011～2013
課題番号 : 23592681
研究分野 : 医歯薬学
科研費の分科・細目 : 外科系臨床医学・救急医学