tetano
Editor, Senior Moderator
J Virol. 2012 Sep 5. [Epub ahead of print]
Type I IFN induction during influenza infection increases the susceptibility to secondary S. pneumoniae Infection by negative regulation of γδ T cells.
Li W, Moltedo B, Moran TM.
Source
Department of Microbiology and Immunology Institute, Mount Sinai School of Medicine, New York, NY 10029, USA.
Abstract
The majority of deaths following influenza infection result from secondary bacterial superinfection, most commonly caused by Streptococcus pneumoniae. Several models have been proposed to explain how primary respiratory viral infections exacerbate secondary bacterial disease but the mechanistic explanations have been contradictory. In this study mice were infected with S. pneumoniae at different days after primary influenza A/X31 virus infection. Our findings show that the induction of type I IFNs during a primary non-lethal influenza infection is sufficient to promote a deadly S.pneumoniae secondary infection. Moreover, mice deficient in type I interferon receptor (IFNAR KO) effectively cleared the secondary bacterial infection from their lungs, increased the recruitment of neutrophils and demonstrated an enhanced innate expression of IL-17 relative to wild type mice. Lung γδ T cells were responsible for almost all IL-17 production and their function is compromised during secondary S.pneumoniae infection of WT but not IFNAR KO mice. Adoptive transfer of γδ T cells from IFNAR KO mice reduced the susceptibility to secondary S.pneumoniae infection in the lung of WT mice. Altogether, our study highlights the importance of type I interferon as a key master regulator that is exploited by opportunistic pathogens such as S.pneumoniae. Our findings may be utilized to design effective preventive and therapeutic strategies that may be beneficial for coinfected patients during influenza epidemics.
PMID:
22951826
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/22951826
Type I IFN induction during influenza infection increases the susceptibility to secondary S. pneumoniae Infection by negative regulation of γδ T cells.
Li W, Moltedo B, Moran TM.
Source
Department of Microbiology and Immunology Institute, Mount Sinai School of Medicine, New York, NY 10029, USA.
Abstract
The majority of deaths following influenza infection result from secondary bacterial superinfection, most commonly caused by Streptococcus pneumoniae. Several models have been proposed to explain how primary respiratory viral infections exacerbate secondary bacterial disease but the mechanistic explanations have been contradictory. In this study mice were infected with S. pneumoniae at different days after primary influenza A/X31 virus infection. Our findings show that the induction of type I IFNs during a primary non-lethal influenza infection is sufficient to promote a deadly S.pneumoniae secondary infection. Moreover, mice deficient in type I interferon receptor (IFNAR KO) effectively cleared the secondary bacterial infection from their lungs, increased the recruitment of neutrophils and demonstrated an enhanced innate expression of IL-17 relative to wild type mice. Lung γδ T cells were responsible for almost all IL-17 production and their function is compromised during secondary S.pneumoniae infection of WT but not IFNAR KO mice. Adoptive transfer of γδ T cells from IFNAR KO mice reduced the susceptibility to secondary S.pneumoniae infection in the lung of WT mice. Altogether, our study highlights the importance of type I interferon as a key master regulator that is exploited by opportunistic pathogens such as S.pneumoniae. Our findings may be utilized to design effective preventive and therapeutic strategies that may be beneficial for coinfected patients during influenza epidemics.
PMID:
22951826
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/22951826