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. Author manuscript; available in PMC: 2010 Sep 1.
Published in final edited form as: J Immunol. 2009 Aug 10;183(5):3400–3408. doi: 10.4049/jimmunol.0900838

Figure 1.

Figure 1

GC frass-induced experimental allergic asthma in TLR2-deficient mice. C57Bl/6 and TLR2-deficient mice were sensitized on day 0 and 7 with an intraperitoneal injection of PBS or GC frass (10 μg/ml) bound to alum. On day 14 and 19, an intratracheal inhalation was performed using PBS (40 μl) or GC frass (40 μg/40 μl). On day 22, mice were anesthetized and acetylcholine was injected after establishment of a stable airway pressure. Blood was collected and BAL fluid was harvested. In all cases, means ± SEM (n=6-8 mice per group) were reported. Statistical significance was determined by ANOVA. A. AHR was measured as airway pressure time index (APTI) in cm-H2O × sec -1 (compared to PBS *p=0.019, **p=0.003). B. IL-5 levels (compared to PBS *p=0.001, **p=0.004). C. IL-13 levels (compared to PBS *p=0.004, **p=0.013). D. Serum IgE levels (compared to PBS *p<0.001; compared to GC frass **p<0.001). E. Frass-specific IgE levels (compared to PBS *p<0.001; compared to GC frass **p=0.019). F. Serum IgG1 levels (compared to PBS *p0.025, ** p<0.001; compared to GC frass ***p=0.007).