セキ　マサフミ   SEK Masafumi   関　雅文    所属   埼玉医科大学  医学部 国際医療センター　感染症科・感染制御科    職種   教授
論文種別	学術雑誌(原著)
言語種別	英語
査読の有無	査読あり
表題	Increase of apoptosis in a murine model for severe pneumococcal pneumonia during influenza A virus infection.
掲載誌名	正式名：Japanese journal of infectious diseases ISSNコード：13446304
巻・号・頁	64(6),451-7頁
著者・共著者	Kosuke Kosai,Masafumi Seki,Akitaka Tanaka,Yoshitomo Morinaga,Yoshifumi Imamura,Koichi Izumikawa,Hiroshi Kakeya,Yoshihiro Yamamoto,Katsunori Yanagihara,Kazunori Tomono,Shigeru Kohno
発行年月	2011
概要	The mechanisms of severe pneumonia caused by co-infection of bacteria and influenza A virus (IAV) have not been fully elucidated. We examined apoptosis and inflammatory responses in a murine model for pneumococcal pneumonia during IAV infection. Inflammation, respiratory epithelium apoptosis, and inflammatory-cell infiltration increased in a time dependent manner in the lungs of mice co-infected with Streptococcus pneumoniae and IAV, in comparison with those infected with either S. pneumoniae or IAV. According to appearance of terminal deoxynucleotidyl transferase dUTP-mediated nick-end labeling positive cells, caspases-3 and -8 were activated 24 h after S. pneumoniae infection, and caspase-3 activation decreased after 48 h, whereas inflammatory cytokine levels continued to increase in co-infected mice. In contrast, in mice infected with either IAV or S. pneumoniae, apoptosis and activation of factors related to caspase-3 peaked at 48 h. Furthermore, Fas-associated death domain was significantly expressed in the lungs of co-infected mice 24 h after S. pneumoniae infection. These data suggest that early onset of apoptosis and its related factors play important roles in fulminant pne
PMID	22116322