title: Increase of apoptosis in a murine model for severe pneumococcal pneumonia during influenza A virus infection.
abstract: 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 pneumonia resulting from  bacterial pneumonia complicated by co-infection with influenza virus.
authors: Second Department of Internal Medicine, Nagasaki University, Nagasaki 852-8501, Japan.
authors: Kosuke
authors: K
authors: Kosai
authors: Masafumi
authors: M
authors: Seki
authors: Akitaka
authors: A
authors: Tanaka
authors: Yoshitomo
authors: Y
authors: Morinaga
authors: Yoshifumi
authors: Y
authors: Imamura
authors: Koichi
authors: K
authors: Izumikawa
authors: Hiroshi
authors: H
authors: Kakeya
authors: Yoshihiro
authors: Y
authors: Yamamoto
authors: Katsunori
authors: K
authors: Yanagihara
authors: Kazunori
authors: K
authors: Tomono
authors: Shigeru
authors: S
authors: Kohno
mesh_terms: D000818:Animals; D017209:Apoptosis; D053148:Caspase 3 / Q000032:analysis; D053181:Caspase 8 / Q000032:analysis; D060085:Coinfection / Q000382:microbiology / Q000473:pathology / Q000821:virology; D016207:Cytokines / Q000378:metabolism; D004195:Disease Models, Animal; D020287:In Situ Nick-End Labeling; D009980:Influenza A virus / Q000472:pathogenicity; D008168:Lung / Q000382:microbiology / Q000473:pathology* / Q000821:virology; D008297:Male; D051379:Mice; D008808:Mice, Inbred CBA; D009976:Orthomyxoviridae Infections / Q000150:complications* / Q000473:pathology* / Q000821:virology; D011018:Pneumonia, Pneumococcal / Q000150:complications* / Q000382:microbiology / Q000473:pathology*; D013296:Streptococcus pneumoniae / Q000472:pathogenicity
chemical_list: D016207:Cytokines; C505526:Casp8 protein, mouse; D053148:Caspase 3; D053181:Caspase 8