• Kosuke Kosai, Masafumi Seki, Akitaka Tanaka, Yoshitomo Morinaga, Yoshifumi Imamura, Koichi Izumikawa, Hiroshi Kakeya, Yoshihiro Yamamoto, Katsunori Yanagihara, Kazunori Tomono, and Shigeru Kohno.
• Second Department of Internal Medicine, Nagasaki University, Nagasaki 852-8501, Japan.
• Jpn. J. Infect. Dis. 2011 Jan 1; 64 (6): 451-7.

AbstractThe 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 pneumonia resulting from bacterial pneumonia complicated by co-infection with influenza virus.

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