The study, published in the current issue of Journal of Clinical Investigation
, details the role of molecules known as type I interferons (IFNs) in mice that are sick with the flu (influenza virus). IFNs, “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.”
The mediators (type I IFNs) impaired this additional immune response because it “decreased production of soluble factors that attract neutrophils, immune cells central to the initial antibacterial immune response, to sites of bacterial infection.”
Most human deaths following infection with influenza occur because the individual develops pneumonia due to secondary infection with bacteria such as Streptococcus pneumoniae.
It is suggested that additional research regarding this newly identified mechanism may, one day, allow for new treatments to combat post-flu pneumonia in humans.