Fig. 1: Treatment with a DP2 antagonist, but not a corticosteroid, ameliorates airway remodeling during a RV-triggered exacerbation of CEA.

A Study design. Seven days old mice were inoculated with PVM and exposed to CRE 3 days later. Mice were re-infected with PVM six weeks later and exposed to CRE weekly for four weeks. Four weeks later, mice were inoculated with RV-1b. Separate groups of mice were treated with a DP2 antagonist (OC000459), DP1 agonist (BW245c), fluticasone, soluble IL-13Rα2 or vehicle. Mice exposed to vehicle instead of virus or allergen were referred to as naïve. Mice were then inoculated with RV-1b and euthanized at 1, 3 and 7 days post infection (dpi). B Lung PGD2 levels. C Representative lung histology of α-smooth muscle actin (SMA) expression. Scale bars = 50 µm. D, E Airway smooth muscle (ASM) area. F, G Collagen deposition. H, I Mucus score. Data are presented as mean ± SEM or box-and-whisker plots showing individual data points with the boxes representing quartiles and whiskers indicating the range and are pooled data from two independent experiments (n = 4–16 mice per group). Statistical significance between different time points or different groups was determined using one-way ANOVA with Dunnett’s multiple comparison test. * denotes p < 0.05, ** denotes p < 0.01 and *** denotes p < 0.001 compared to Vehicle group. # denotes p < 0.05, ## denotes p < 0.01 and ### denotes p < 0.001 compared to RV-infected group at corresponding time point. Source data are provided as a Source Data file.