IL-18 and IL-1 contribute to the induction of Th17 cell–mediated neutrophilic airway inflammation. Mice were treated with 50 μg of OVA or PBS intranasally for 3 day (once per day). Cells in BALF were quantified 24 hours after the last OVA or PBS inhalation. (A) OVA- or PBS-challenged IL-18^+/+ OTII mice (PBS, n = 6; OVA, n = 10), and IL-18^−/− OTII mice (PBS, n = 6; OVA, n = 10). (B) OVA- or PBS-challenged wild-type OTII mice (OTII: PBS, n = 6; OVA, n = 10), IL-1R1^−/− OTII mice (PBS, n = 6; OVA, n = 10), TNF^−/− OTII mice (PBS, n = 6; OVA, n = 10), and IL-1R1^−/− TNF^−/− OTII mice (PBS, n = 6; OVA, n = 10). (C) Cytokine levels in BALF from mice in panels A and B. *P < .01 versus corresponding values for PBS-treated mice; †P < .05 versus corresponding values for OVA-treated IL-18^+/+ OTII mice (A,C) or wild-type OTII mice (B,C). ‡P < .05 versus corresponding values for OVA-treated IL-1R1^−/− OTII mice (B). Data are the average + SD of results pooled from 2 independent experiments, each of which gave similar results.