ITGAM and bacterial infectious disease: Previous studies of post-influenza pneumococcal pneumonia have reported that IFN-γ production is detrimental to secondary bacterial infection [21, 22]; thus, because our results showed that CAM and CAM-treated CD11b+Gr-1+ cells suppress IFN-γ production in post-influenza pneumococcal pneumonia, we hypothesized that IFN-γ might have a detrimental effect on survival in our model mice.