Increase of Apoptosis in a Murine Model for Severe Pneumococcal Pneumonia during Influenza A Virus Infection
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- Kosai Kosuke
- Second Department of Internal Medicine, Nagasaki University, Japan
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- Seki Masafumi
- Second Department of Internal Medicine, Nagasaki University, Japan Division of Infectious Diseases and Prevention, Osaka University Hospital, Japan
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- Tanaka Akitaka
- Second Department of Internal Medicine, Nagasaki University, Japan
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- Morinaga Yoshitomo
- Second Department of Internal Medicine, Nagasaki University, Japan
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- Imamura Yoshifumi
- Second Department of Internal Medicine, Nagasaki University, Japan
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- Izumikawa Koichi
- Second Department of Internal Medicine, Nagasaki University, Japan
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- Kakeya Hiroshi
- Second Department of Internal Medicine, Nagasaki University, Japan
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- Yamamoto Yoshihiro
- Second Department of Internal Medicine, Nagasaki University, Japan
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- Yanagihara Katsunori
- Second Department of Internal Medicine, Nagasaki University, Japan
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- Tomono Kazunori
- Division of Infectious Diseases and Prevention, Osaka University Hospital, Japan
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- Kohno Shigeru
- Second Department of Internal Medicine, Nagasaki University, Japan
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抄録
<p>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.<tt> </tt></p>
収録刊行物
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- Japanese Journal of Infectious Diseases
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Japanese Journal of Infectious Diseases 64 (6), 451-457, 2011-11-30
国立感染症研究所 Japanese Journal of Infectious Diseases 編集委員会
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詳細情報 詳細情報について
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- CRID
- 1390291767791419648
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- NII論文ID
- 120006985192
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- NII書誌ID
- AA1132885X
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- ISSN
- 18842836
- 13446304
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- HANDLE
- 10069/27108
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- NDL書誌ID
- 023365088
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- IRDB
- NDL
- Crossref
- CiNii Articles
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