tetano
Editor, Senior Moderator
Jpn J Infect Dis. 2011 Nov;64(6):451-7.
Increase of Apoptosis in a Murine Model for Severe Pneumococcal Pneumonia during Influenza A Virus Infection.
Kosai K, Seki M, Tanaka A, Morinaga Y, Imamura Y, Izumikawa K, Kakeya H, Yamamoto Y, Yanagihara K, Tomono K, Kohno S.
Source
Second Department of Internal Medicine, Nagasaki University, Nagasaki 852-8501, Japan.
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.
PMID:
22116322
[PubMed - in process]
http://www.ncbi.nlm.nih.gov/pubmed/22116322
Increase of Apoptosis in a Murine Model for Severe Pneumococcal Pneumonia during Influenza A Virus Infection.
Kosai K, Seki M, Tanaka A, Morinaga Y, Imamura Y, Izumikawa K, Kakeya H, Yamamoto Y, Yanagihara K, Tomono K, Kohno S.
Source
Second Department of Internal Medicine, Nagasaki University, Nagasaki 852-8501, Japan.
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.
PMID:
22116322
[PubMed - in process]
http://www.ncbi.nlm.nih.gov/pubmed/22116322