Impact of type I and III interferons on respiratory superinfections due to multidrug-resistant pathogens

Abstract

The increased morbidity and mortality associated with bacterial pneumonias that are acquired following influenza infection are well appreciated by clinicians. One of the major components of the immune response to influenza is the induction of the types I and III interferon cascades, which encompasses the activation of over 300 genes. The immunological consequences of IFN activation, while important for viral clearance, modify the host proinflammatory responses through effects on the inflammasome, Th17 signaling and recruitment of phagocytic cells. IFN signaling affects both susceptibility to subsequent Streptococcus pneumoniae and Staphylococcus aureus infection as well as the intensity of the immune responses associated with pulmonary damage. Appreciation for the effects of IFN activation on anti-bacterial pulmonary defense mechanisms should help to inform therapeutic strategies in an ICU setting.