Since interferon signaling is essential to baseline host antiviral resistance in the lungs [17, 18] , we investigated whether treatment with NTHi lysate was capable of inducing an interferon response. In addition to the robust induction of inflammatory cytokines, we found that NTHi lysate treatment also induces significant increases in lung interferon c levels ( Fig. 2A) . However, unlike IL-6 and TNF, the fulminant influenza infections observed in untreated mice actually induce 4-fold higher levels of interferon c than the NTHi lysate treatment (Fig. 2B ). Presumably this reflects the ongoing antiviral response of the host, in contrast to the better contained infections of the treated mice.