Figure 5.

Rhinovirus exacerbates airway inflammation, airway hyper-responsiveness, mucus production, and T_H1 and T_H2 cytokine responses in a model of acute allergic airway inflammation. OVA-sensitized mice were challenged intranasally with OVA or PBS control and infected with RV-1B (RV-OVA or RV-PBS) or UV-inactivated virus (UV-OVA or UV-PBS). (a) Kinetic analysis of BAL cells showing neutrophils (left) and lymphocytes (right) at the indicated time points after infection, as assessed by differential cell counts. (b) Airway hyper-responsiveness to increasing doses of methacholine (MCH), as assessed at 24 h after infection by Penh area under the curve (AUC) analysis (left). Penh results were confirmed by invasive measures of airway resistance (right). BL, baseline. (c) Muc5AC (left) and Muc5B (right) protein abundance in BAL, as determined by ELISA. Measurement of T_H2 cytokines IL-4 (d) and IL-13 (e) in BAL was performed by quantitative ELISA, and IFN-γ production by lung leukocytes (f) was assessed by ELISpot. All data are expressed as means ± s.e.m. for groups of four mice. *P < 0.05, **P < 0.01 and ***P < 0.001 RV-OVA compared to RV-PBS. ⁺P < 0.05, ⁺⁺P < 0.01 and ⁺⁺⁺P < 0.001 for RV-OVA compared to UV-OVA. ^#P < 0.05 and ^###P < 0.001 for allergic groups (RV-OVA and UV-OVA) compared to controls (UV-PBS).