Lower respiratory tract infections are the leading cause of infectious death worldwide [1] . We have recently shown that Stimulated Innate Resistance (StIR) of the lungs induced by an aerosolized bacterial lysate can protect mice against otherwise fatal bacterial pneumonias [16] . We show here that the same treatment can prevent viral pneumonia, despite induction of lung inflam- mation of greater magnitude than that observed with lethal infection. Influenza-induced excessive and/or dysregulated lung inflammation has been recently described as a mechanism by which pandemic infections cause mortality [10, 11, 12, 13] . Consequent to these observations, considerable effort has been invested in attempts to improve outcomes of influenza-infected mice through genetic and pharmacologic suppression of inflammatory cytokine production [12, 20, 21, 22] . In contrast, our current and previous data demonstrate robust inflammation associated with the induction of protective host responses (Fig. 3a-d) . As we have previously shown that repetitive treatments result in diminishing inflammatory responses without loss of protection, it is possible that the cytokines themselves are not responsible for the protective effect. However, like our previous observations with protection against bacterial pathogens [16] , the pro-inflammatory pretreatment resulted in a significant reduction in pathogen burden, here represented by decreased viral titers (Fig. 1d) . As interferon signaling is associated with survival of viral and bacterial infections, the observation of augmented type I and II interferon signaling after NTHi lysate treatment ( Figure 3A -B, Table 1 ) supports our hypothesis that this is also an important element of anti-viral StIR, and we will explore this in the future.