tetano
Editor, Senior Moderator
Clin Vaccine Immunol. 2013 May 1. [Epub ahead of print]
TLR4 agonistic antibody promotes innate immunity against severe pneumonia induced by co-infection with influenza virus and Streptococcus pneumoniae.
Tanaka A, Nakamura S, Seki M, Fukudome K, Iwanaga N, Imamura Y, Miyazaki T, Izumikawa K, Kakeya H, Yanagihara K, Kohno S.
Source
Department of Molecular Microbiology and Immunology, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki University School of Medicine, Nagasaki, Japan.
Abstract
Co-infection with bacteria is a major cause of mortality during influenza epidemics. Recently, toll-like receptor (TLR) agonists have been 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 co-infection 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 rate and body weight loss were significantly improved by UT12 administration. Additionally, the production of inflammatory mediators was significantly suppressed by 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 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 (MCP)-1 production. Collectively, these findings indicated that UT12 promoted pulmonary innate immunity and may reduce the severity of severe pneumonia induced by co-infection with influenza virus and S. pneumoniae. This immunomodulatory effect of UT12 improves the prognosis of secondary pneumococcal pneumonia and makes it an attractive candidate for treating severe infectious diseases.
PMID:
23637040
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/23637040
TLR4 agonistic antibody promotes innate immunity against severe pneumonia induced by co-infection with influenza virus and Streptococcus pneumoniae.
Tanaka A, Nakamura S, Seki M, Fukudome K, Iwanaga N, Imamura Y, Miyazaki T, Izumikawa K, Kakeya H, Yanagihara K, Kohno S.
Source
Department of Molecular Microbiology and Immunology, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki University School of Medicine, Nagasaki, Japan.
Abstract
Co-infection with bacteria is a major cause of mortality during influenza epidemics. Recently, toll-like receptor (TLR) agonists have been 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 co-infection 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 rate and body weight loss were significantly improved by UT12 administration. Additionally, the production of inflammatory mediators was significantly suppressed by 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 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 (MCP)-1 production. Collectively, these findings indicated that UT12 promoted pulmonary innate immunity and may reduce the severity of severe pneumonia induced by co-infection with influenza virus and S. pneumoniae. This immunomodulatory effect of UT12 improves the prognosis of secondary pneumococcal pneumonia and makes it an attractive candidate for treating severe infectious diseases.
PMID:
23637040
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/23637040