tetano
Editor, Senior Moderator
Mucosal Immunol. 2012 Feb 1. doi: 10.1038/mi.2012.2. [Epub ahead of print]
Essential role of IL-6 in protection against H1N1 influenza virus by promoting neutrophil survival in the lung.
Dienz O, Rud JG, Eaton SM, Lanthier PA, Burg E, Drew A, Bunn J, Suratt BT, Haynes L, Rincon M.
Source
1] Department of Medicine/Immunobiology, The University of Vermont, Burlington, Vermont, USA [2] These authors contributed equally to this work.
Abstract
Influenza virus infection is considered a major worldwide public health problem. Seasonal infections with the most common influenza virus strains (e.g., H1N1) can usually be resolved, but they still cause a high rate of mortality. The factors that influence the outcome of the infection remain unclear. Here, we show that deficiency of interleukin (IL)-6 or IL-6 receptor is sufficient for normally sublethal doses of H1N1 influenza A virus to cause death in mice. IL-6 is necessary for resolution of influenza infection by protecting neutrophils from virus-induced death in the lung and by promoting neutrophil-mediated viral clearance. Loss of IL-6 results in persistence of the influenza virus in the lung leading to pronounced lung damage and, ultimately, death. Thus, we demonstrate that IL-6 is a vital innate immune cytokine in providing protection against influenza A infection. Genetic or environmental factors that impair IL-6 production or signaling could increase mortality to influenza virus infection.Mucosal Immunology advance online publication 1 February 2012. doi:10.1038/mi.2012.2.
PMID:
22294047
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/22294047
Essential role of IL-6 in protection against H1N1 influenza virus by promoting neutrophil survival in the lung.
Dienz O, Rud JG, Eaton SM, Lanthier PA, Burg E, Drew A, Bunn J, Suratt BT, Haynes L, Rincon M.
Source
1] Department of Medicine/Immunobiology, The University of Vermont, Burlington, Vermont, USA [2] These authors contributed equally to this work.
Abstract
Influenza virus infection is considered a major worldwide public health problem. Seasonal infections with the most common influenza virus strains (e.g., H1N1) can usually be resolved, but they still cause a high rate of mortality. The factors that influence the outcome of the infection remain unclear. Here, we show that deficiency of interleukin (IL)-6 or IL-6 receptor is sufficient for normally sublethal doses of H1N1 influenza A virus to cause death in mice. IL-6 is necessary for resolution of influenza infection by protecting neutrophils from virus-induced death in the lung and by promoting neutrophil-mediated viral clearance. Loss of IL-6 results in persistence of the influenza virus in the lung leading to pronounced lung damage and, ultimately, death. Thus, we demonstrate that IL-6 is a vital innate immune cytokine in providing protection against influenza A infection. Genetic or environmental factors that impair IL-6 production or signaling could increase mortality to influenza virus infection.Mucosal Immunology advance online publication 1 February 2012. doi:10.1038/mi.2012.2.
PMID:
22294047
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/22294047