Since a variety of cytokines, chemokines and growth factors were produced in the lungs during microbial infection, which contributed to recruit and activate inflammatory cells with concomitant clearance of microbes (Ward 2012), we next examined whether there were any differences in the levels of lung inflammatory mediators in influenza-infected WT and IL-27R-deficient mice upon secondary S. pneumoniae challenge. The gene discussed is IL27RA; the disease is influenza.