Fig. 3.

Early-life infection with EV-A71 enhances allergic asthma responses to HDM allergen. A Protocol 2 experimental scheme. Thirty-five-day-old EV-A71–infected or mock-infected mice were intranasally and intratracheally challenged with PBS or HDM allergen. B Total IgE and C HDM-specific IgE serum concentrations were determined using ELISA (n = 15 mice, *p < 0.05 and **p < 0.01, one-way ANOVA with the Bonferroni multiple-comparison test). D Airway resistance (Rrs) and E elastane (Ers) levels in response to increasing doses of aerosolized methacholine were calculated using a flexiVent FX system (n = 15 mice, *p < 0.05 and **p < 0.01, two-way ANOVA with the Bonferroni posttest). F Total cell, eosinophil, neutrophil, lymphocyte, and macrophage counts in the BALF were determined (n = 15 mice, *p < 0.05 and **p < 0.01, one-way ANOVA with the Bonferroni multiple-comparison test). G Lung histology. Lung sections were stained with H&E, PAS, or an anti-EV-A71 antibody. H TARC production in the BALF was evaluated using ELISA (n = 15 mice, *p < 0.05, one-way ANOVA with the Bonferroni multiple-comparison test). I IL-4⁺, IL-5⁺, IL-13⁺, and IL-17A⁺CD4⁺ T cell percentages in lung single-cell suspensions were determined using FACS (n = 15 mice, *p < 0.05 and **p < 0.01, one-way ANOVA with the Bonferroni multiple-comparison test). The findings represent pooled data from three independent experiments