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Toll-Like Receptor 4 Agonistic Antibody Promotes Innate Immunity against Severe Pneumonia Induced by Coinfection with Influenza Virus and Streptococcus pneumoniae
http://hdl.handle.net/10069/34032
http://hdl.handle.net/10069/340325ad9f2a6-ee53-45e7-9a07-46feec563d9f
名前 / ファイル | ライセンス | アクション |
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CVI20_977.pdf (6.6 MB)
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Item type | 学術雑誌論文 / Journal Article(1) | |||||
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公開日 | 2014-02-01 | |||||
タイトル | ||||||
タイトル | Toll-Like Receptor 4 Agonistic Antibody Promotes Innate Immunity against Severe Pneumonia Induced by Coinfection with Influenza Virus and Streptococcus pneumoniae | |||||
言語 | ||||||
言語 | eng | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | Secondary bacterial pneumonia | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | innate immunity | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | influenza virus | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | Streptococcus pneumoniae | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | macrophage | |||||
資源タイプ | ||||||
資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||
資源タイプ | journal article | |||||
著者 |
Tanaka, Akitaka
× Tanaka, Akitaka× Nakamura, Shigeki× Seki, Masafumi× Fukudome, Kenji× Iwanaga, Naoki× Imamura, Yoshifumi× Miyazaki, Taiga× Izumikawa, Koichi× Kakeya, Hiroshi× Yanagihara, Katsunori× Kohno, Shigeru |
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抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | Coinfection with bacteria is a major cause of mortality during influenza epidemics. Recently, Toll-like receptor (TLR) agonists were shown to have immunomodulatory functions. In the present study, we investigated the effectiveness and mechanisms of the new TLR4 agonistic monoclonal antibody UT12 against secondary pneumococcal pneumonia induced by coinfection with influenza virus in a mouse model. Mice were intranasally inoculated with Streptococcus pneumoniae 2 days after influenza virus inoculation. UT12 was intraperitoneally administered 2 h before each inoculation. Survival rates were significantly increased and body weight loss was significantly decreased by UT12 administration. Additionally, the production of inflammatory mediators was significantly suppressed by the administration of UT12. In a histopathological study, pneumonia in UT12-treated mice was very mild compared to that in control mice. UT12 increased antimicrobial defense through the acceleration of macrophage recruitment into the lower respiratory tract induced by c-Jun N-terminal kinase (JNK) and nuclear factor kappaB (NF-κB) pathway- dependent monocyte chemoattractant protein 1 (MCP-1) production. Collectively, these findings indicate that UT12 promoted pulmonary innate immunity and may reduce the severity of severe pneumonia induced by coinfection with influenza virus and S. pneumoniae. This immunomodulatory effect of UT12 improves the prognosis of secondary pneumococcal pneumonia and makes UT12 an attractive candidate for treating severe infectious diseases. | |||||
書誌情報 |
Clinical and Vaccine Immunology 巻 20, 号 7, p. 977-985, 発行日 2013-07 |
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出版者 | ||||||
出版者 | American Society for Microbiology | |||||
ISSN | ||||||
収録物識別子タイプ | ISSN | |||||
収録物識別子 | 15566811 | |||||
DOI | ||||||
関連タイプ | isVersionOf | |||||
識別子タイプ | DOI | |||||
関連識別子 | 10.1128/CVI.00010-13 | |||||
権利 | ||||||
権利情報 | © 2013, American Society for Microbiology. All Rights Reserved. | |||||
著者版フラグ | ||||||
出版タイプ | AM | |||||
出版タイプResource | http://purl.org/coar/version/c_ab4af688f83e57aa | |||||
引用 | ||||||
内容記述タイプ | Other | |||||
内容記述 | Clinical and Vaccine Immunology, 20(7), pp.977-985; 2013 |