Figure 6

GC frass proteases do not regulate airway inflammation and airway hyperresponsiveness. BALB/c mice were sensitized on day 0 and 7 with an intraperitoneal injection of PBS, aprotinin-treated PBS, GC frass, or GC frass pretreated with aprotinin (10 μg/ml) and then bound to alum. On days 14 and 19, an intratracheal inhalation was performed using PBS, PBS pretreated with aprotinin, GC frass (40 μg) or GC frass pretreated with aprotinin. On day 22, mice were anesthetized acetylcholine was injected after establishment of a stable airway pressure. In all cases the data are expressed as mean ± SEM and represent 8 mice per group and statistical significance determined by ANOVA. A. AHR was measured as airway pressure time index (APTI) in cm-H₂O × sec ^-1 (compared to PBS * p < 0.001). B. Serum IgE levels were analyzed by ELISA (compared to PBS *p < 0.001, compared to GC frass **p < 0.002). C-F. Lungs from the mice were excised, and cells dissociated and maintained in a single suspension culture for 3 days in the presence of Con A (10 μg/ml). C. IL-5 levels (compared to PBS *p < 0.05). D. IL-13 levels (compared to PBS *p < 0.001). E. IL-17A levels. F. IFNγ levels (compared to PBS *p < 0.05).