tetano
Editor, Senior Moderator
Antiviral Res. 2013 May 27. pii: S0166-3542(13)00138-1. doi: 10.1016/j.antiviral.2013.05.007. [Epub ahead of print]
Type I interferon limits influenza virus-induced acute lung injury by regulation of excessive inflammation in mice.
Arimori Y, Nakamura R, Yamada H, Shibata K, Maeda N, Kase T, Yoshikai Y.
Source
Division of Host Defense, Medical Institute of Bioregulation, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan.
Abstract
Anti-viral immune responses play as a double edged sword in resolution of infection and pathogenesis of acute lung injury caused by infection with highly pathogenic influenza A viruses. Here we show that type I interferons (IFNs) are important in protection against acute influenza A virus infection not only via their antiviral activity but also via their anti-inflammatory activity. IFN α receptor (IFNAR) knock-out (KO) mice exhibited increased mortality and morbidity with higher viral load after infection with influenza virus A/FM/1/47 (H1N1, a mouse-adapted strain) compared with wild-type (WT) mice, though the viruses were finally eliminated in both groups. The levels of proinflammatory cytokines in the lungs were significantly higher, while the level of IL-10 in the lungs was significantly lower in IFNAR KO mice than in WT mice during the course of infection. Restoration of IL-10 during an ongoing virus infection significantly reduced the levels of proinflammatory cytokines and improved mortality of IFNAR KO mice. These results suggest that type I IFNs are responsible not only for direct resolution of viral load but also for suppression of immunopathology caused by influenza A virus through IL-10 production.
Copyright ? 2013. Published by Elsevier B.V.
PMID:
23721943
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/23721943
Type I interferon limits influenza virus-induced acute lung injury by regulation of excessive inflammation in mice.
Arimori Y, Nakamura R, Yamada H, Shibata K, Maeda N, Kase T, Yoshikai Y.
Source
Division of Host Defense, Medical Institute of Bioregulation, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan.
Abstract
Anti-viral immune responses play as a double edged sword in resolution of infection and pathogenesis of acute lung injury caused by infection with highly pathogenic influenza A viruses. Here we show that type I interferons (IFNs) are important in protection against acute influenza A virus infection not only via their antiviral activity but also via their anti-inflammatory activity. IFN α receptor (IFNAR) knock-out (KO) mice exhibited increased mortality and morbidity with higher viral load after infection with influenza virus A/FM/1/47 (H1N1, a mouse-adapted strain) compared with wild-type (WT) mice, though the viruses were finally eliminated in both groups. The levels of proinflammatory cytokines in the lungs were significantly higher, while the level of IL-10 in the lungs was significantly lower in IFNAR KO mice than in WT mice during the course of infection. Restoration of IL-10 during an ongoing virus infection significantly reduced the levels of proinflammatory cytokines and improved mortality of IFNAR KO mice. These results suggest that type I IFNs are responsible not only for direct resolution of viral load but also for suppression of immunopathology caused by influenza A virus through IL-10 production.
Copyright ? 2013. Published by Elsevier B.V.
PMID:
23721943
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/23721943