IL-17 promotes, but IFN-γ suppresses, neutrophilic airway inflammation. Mice were treated with 50 μg of OVA or PBS intranasally for 3 days (once per day) (A-C) or 10 μg of LPS intranasally (D). Cells in BALF were quantified 24 hours after the last OVA, PBS, or LPS inhalation. (A) OVA or PBS-challenged IFN-γ^+/+ OTII mice (PBS, n = 16; OVA, n = 21), and IFN-γ^−/− OTII mice (PBS, n = 6; OVA, n = 14). (B) OVA- or PBS-challenged IL-17^+/+ OTII mice (PBS, n = 12; OVA, n = 14), and IL-17^−/− OTII mice (PBS, n = 7; OVA, n = 14). (C) Cytokine levels in BALF obtained 24 hours after the last OVA or PBS inhalation in mice shown in panels A and B. (D) LPS-challenged wild-type mice (n = 15), OTII mice (n = 7), IL-17^−/− mice (n = 15), IFN-γ^−/− mice (n = 12), and Rag-1^−/− mice (n = 7). *P < .01 versus corresponding values for PBS-treated mice; †P < .01 versus corresponding values for OVA-treated IFN-γ^+/+ OTII mice (A,C) or OVA-treated IL-17^+/+ OTII mice (B,C). *P < .01 versus corresponding values for LPS-treated mice of any other genotype (D). Data are the average + SD of results pooled from 2 or 3 independent experiments, all of which gave similar results.