Based on our in vitro infection experiments with neutrophils from TLR2-, NOD2-, or FPR1-deficient mice, there was decreased IL-1β production compared with neutrophils from wt mice (Fig. 6A), suggesting these each of these PRRs on neutrophils directly contribute to the production of IL-1β in response to S. aureus. The gene discussed is FPR1; the disease is infection.