Fig. 8

Inhibition of NOX2 oxidase increases expression of Type I IFN and IL-1β, and antibody production to influenza A virus infection. a Alveolar macrophages from WT and Nox2^−/y mice were either left untreated (naïve) or infected with HKx31 influenza A virus (MOI of 10) for analysis of IFN-β, IL-1β, TNF-α, and IL-6 mRNA expression by QPCR after 24 h (n = 8). b, c WT and Nox2^−/y mice were infected with live HKx31 influenza A virus (1 × 10⁵ PFU per mouse) and b cytokine mRNA expression and IFN-β protein expression in c BALF or d serum were assessed 3 days later (n = 5). e–i WT and Nox2^−/y mice were infected with inactivated HKx31 influenza A virus (equivalent to 1 × 10⁴ PFU per mouse) for measurements at day 7 of: e body weight; f airway inflammation and differential cell counts (i.e., macrophages, neutrophils, and lymphocytes); g cytokine expression in whole lung (responses are shown as fold change relative to GAPDH) and h serum and i BALF antibody levels (n = 6). Data are shown as mean ± SE. a Kruskal–Wallis test with Dunn’s post hoc for multiple comparisons. b–i Unpaired t-test; statistical significance taken when the P < 0.05. *P < 0.05. **P < 0.01