セキ　マサフミ   SEK Masafumi   関　雅文    所属   埼玉医科大学  医学部 国際医療センター　感染症科・感染制御科    職種   教授
論文種別	学術雑誌(原著)
言語種別	英語
査読の有無	査読あり
表題	Toll-like receptor 4 agonistic antibody promotes innate immunity against severe pneumonia induced by coinfection with influenza virus and Streptococcus pneumoniae.
掲載誌名	正式名：Clinical and vaccine immunology : CVI ISSNコード：15566811
巻・号・頁	20(7),977-85頁
著者・共著者	Akitaka Tanaka,Shigeki Nakamura,Masafumi Seki,Kenji Fukudome,Naoki Iwanaga,Yoshifumi Imamura,Taiga Miyazaki,Koichi Izumikawa,Hiroshi Kakeya,Katsunori Yanagihara,Shigeru Kohno
発行年月	2013/07
概要	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 significantlysuppressed 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,
DOI	10.1128/CVI.00010-13
PMID	23637040