@article{oai:nagasaki-u.repo.nii.ac.jp:00012911,
 author = {Kosai, Kosuke and Seki, Masafumi and Tanaka, Akitaka and Morinaga, Yoshitomo and Imamura, Yoshifumi and Izumikawa, Koichi and Kakeya, Hiroshi and Yamamoto, Yoshihiro and Yanagihara, Katsunori and Tomono, Kazunori and Kohno, Shigeru},
 issue = {6},
 journal = {Japanese Journal of Infectious Diseases},
 month = {},
 note = {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 dUTPmediated nick-end labeling positive cells, caspase-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 pneumonia resulting from bacterial pneumonia complicated by co-infection with influenza virus., Japanese Journal of Infectious Diseases, 64(6), pp.451-457; 2011},
 pages = {451--457},
 title = {Increase of apoptosis in a murine model for severe pneumococcal pneumonia during influenza A virus infection},
 volume = {64},
 year = {2011}
}