SLPI and viral infectious disease: Consistent with our hypothesis that MUC5AC drives neutrophil elastase–mediated cleavage of AMPs and subsequently increases bacterial loads, we also observed that exogenous MUC5AC increased RV induction of neutrophil elastase (Figure 4J), suppressed RV induction of SLPI (Figure 4K), and augmented lung bacterial loads during viral infection (Figure 4L).