tetano
Editor, Senior Moderator
J Virol. 2010 Mar 24. [Epub ahead of print]
Interleukin-15 is critical in the pathogenesis of influenza A virus-induced acute lung injury.
Nakamura R, Maeda N, Shibata K, Yamada H, Kase T, Yoshikai Y.
Division of Host Defense, Research Center for Prevention of Infectious Diseases, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan; Division of Bioinformatics, Digital Medicine Initiative, Kyushu University, Fukuoka, Japan; Osaka Prefectural Institute of Public Health, Osaka, Japan.
Highly pathogenic influenza A viruses cause acute severe pneumonia, to which the occurrence of "cytokine storm" has been proposed to contribute. Here we show that interleukin (IL)-15 knock out (KO) mice exhibited reduced mortality after infection with influenza virus A/FM/1/47 (H1N1, a mouse-adapted strain) albeit no difference in the viral titer from control mice. There were significantly fewer antigen-specific CD44(+)CD8(+) T cells in the lungs of infected IL-15KO mice and adoptive transfer of the CD8(+) T cells deteriorated the survival of IL-15KO mice following influenza infection. Mice deficient in beta2-microglobulin by gene targeting and those depleted of CD8(+) T cells by in vivo administration of anti-CD8 monoclonal antibody displayed a reduced mortality rate after infection. These results indicate that IL-15-dependent CD8(+) T cells are at least partly responsible for the pathogenesis of acute pneumonia caused by influenza A virus.
http://www.ncbi.nlm.nih.gov/pubmed/20335267
Interleukin-15 is critical in the pathogenesis of influenza A virus-induced acute lung injury.
Nakamura R, Maeda N, Shibata K, Yamada H, Kase T, Yoshikai Y.
Division of Host Defense, Research Center for Prevention of Infectious Diseases, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan; Division of Bioinformatics, Digital Medicine Initiative, Kyushu University, Fukuoka, Japan; Osaka Prefectural Institute of Public Health, Osaka, Japan.
Highly pathogenic influenza A viruses cause acute severe pneumonia, to which the occurrence of "cytokine storm" has been proposed to contribute. Here we show that interleukin (IL)-15 knock out (KO) mice exhibited reduced mortality after infection with influenza virus A/FM/1/47 (H1N1, a mouse-adapted strain) albeit no difference in the viral titer from control mice. There were significantly fewer antigen-specific CD44(+)CD8(+) T cells in the lungs of infected IL-15KO mice and adoptive transfer of the CD8(+) T cells deteriorated the survival of IL-15KO mice following influenza infection. Mice deficient in beta2-microglobulin by gene targeting and those depleted of CD8(+) T cells by in vivo administration of anti-CD8 monoclonal antibody displayed a reduced mortality rate after infection. These results indicate that IL-15-dependent CD8(+) T cells are at least partly responsible for the pathogenesis of acute pneumonia caused by influenza A virus.
http://www.ncbi.nlm.nih.gov/pubmed/20335267