Recently, similar to our results, Aegerter et al. found that H3N2 virus preceding 28-day infection also increased host resistance to secondary pneumococcal infection in terms of bacterial loads and mortality in C57BL/6 mice, and this prolonged antibacterial protection was attributed to a population of monocyte-derived alveolar macrophages that produce increased IL-6 (49). Here, IL6 is linked to pneumococcal infection.