RSV infection increases the expression of antiviral genes, and the inhibition of NOS-2 abrogates the protection conferred by eosinophils. (A) FACS-purified splenic eosinophils were isolated from naive hypereosinophilic mice (▩) or hypereosinophilic (■) and hypereosinophilic MyD88-deficient (▨) mice at 1 dpi, and expression of indicated genes were analyzed by quantitative RT-PCR. All quantitative assessments were normalized to HPRT, and fold induction was calculated relative to naive hypereosinophilic mice. *Comparison between naive and RSV inoculated hypereosinophilic mice. #Comparison between RSV-inoculated hypereosinophilic and hypereosinophilic MyD88^−/− mice. (B) WT (○) and hypereosinophilic (●) mice were inoculated, lung samples were collected at the indicated times after infection, and expression of indicated genes were analyzed by quantitative RT-PCR. (C) WT and hypereosinophilic mice were pretreated with L-NMA (■) or D-NMA (▩) prior to inoculation with RSV. Lung viral titer was measured at 3 dpi (n = 3-6 mice). *P < .05; #P < .05; **P < .01; ##P < .01; ***P < .001; ###P < .001. Error bars are SEM.