June 8, 2009 How infection with influenza virus makes an individual sensitive to pneumonia-causing bacterial infections is clinically important but not well understood. New research now indicates that key mediators of the antiviral immune response initiated by infection with influenza virus impair the ability of mice to mount an adequate immune response to subsequent pneumonia-causing bacterial infection. These data might provide a new avenue of research for those developing ways to combat pneumonia following infection with influenza virus.
Complications following infection with the virus that causes flu (influenza virus) are one of the top ten causes of death in the United States. Although infection with influenza virus can directly cause death, many deaths following infection with influenza virus occur because the individual develops pneumonia due to secondary infection with bacteria such as Streptococcus pneumoniae. How influenza makes individuals more sensitive to pneumonia-causing secondary bacterial infections is not well understood. However, Jane Deng and colleagues, at the University of California, Los Angeles, have now determined, through studies in mice, one mechanism by which influenza might sensitize individuals to secondary bacterial pneumonia.
In the study, it was found that molecules known as type I IFNs, which are key mediators of the antiviral immune response initiated by infection with influenza virus, impaired the ability of mice to mount an adequate immune response to subsequent pneumonia-causing bacterial infection. In particular, the type I IFNs decreased production of soluble factors that attract neutrophils, immune cells central to the initial antibacterial immune response, to sites of bacterial infection. The authors therefore suggest that the pathway uncovered in their study might provide a new avenue of research for those developing ways to combat pneumonia following infection with influenza virus.
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- Type I IFNs mediate development of postinfluenza bacterial pneumonia in mice. Journal of Clinical Investigation, June 1, 2009
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