Fig. 4
Ovalbumin-sensitized rats demonstrate increased airway remodeling, inflammatory markers, airway resistance and plasma LPA. a OVA-sensitization protocol (see Methods, OVA Cohort 1). b–e Typical asthmatic airway disease occurred in the OVA-sensitized rats (right c, e) compared to the naive group (left b, d) as indicated by the heightened presence of goblet cells (appearing pink with Periodic acid-Schiffs reagent; b, c) and thickening of airway smooth muscle (appearing brown when immuno-stained for smooth muscle actin; d, e). f qPCR of IL4, eotaxin (CCL11) and house-keeping gene β-actin for OVA (red) and naive (open) rats with calculated change in gene expression magnitude (2−∆CTT68). CT: cycles threshold. OVA vs naive CT for IL4-independent t-test, t11 = 73.271, ***p < 0.00001; CCL11-independent t-test: t12 = 6.369, ***p < 0.0001; and β-actin-independent t-test: t12 = 0.403, p = 0.694. g Bradykinin increases RL in OVA animals only (red; F1,51 (two-way RM ANOVA) = 69.224, p < 0.001). Holm–Šidák post hoc: bradykinin increases RL in OVA animals, ***p < 0.001; but not naive rats (p = 0.40). Prior to bradykinin RL in naive (open) and OVA rats is not significantly different (p = 0.08), following bradykinin RL is greater in OVA compared to naive rats (***p < 0.001). h Bradykinin increases LPA in OVA animals only (F1,55 (two-way RM ANOVA) = 6.19, p = 0.02). Holm–Šidák post hoc: bradykinin increases LPA in OVA animals, ***p < 0.001; bradykinin has no effect on LPA in naive rats (p = 0.21), LPA in naive and OVA rats prior to bradykinin are not significantly different (p = 0.58); but LPA in OVA rats is greater than naive rats following bradykinin (**p = 0.01) (g, h See Methods, OVA Cohort 1). All data are presented as mean ± sem
