Fig. 2.

Allergic sensitization and inflammatory response to chronic HDM is unaltered with EGFR inhibition. A: sensitization was assessed by measurement of total IgG1, total IgE, and HDM-specific (HDM Sp) IgG1 and IgE in bronchoalveolar lavage fluid (BALF) from mice treated with intranasal HDM or saline for 6 wk. HDM-treated groups also included wild-type (WT) mice, erlotinib-treated WT mice, and transgenic mice expressing a mutant dominant negative epidermal growth factor receptor in the lung epithelium (EGFR-M). Increases in total IgG1, total IgE, and HDM-specific IgG1 were similar in all HDM-treated groups. HDM-specific IgE was increased in HDM-treated WT mice and EGFR-M mice, but not the erlotinib-treated group; *P < 0.05 vs. saline control group; +P < 0.05 vs. WT saline. Data were derived from 5–13 animals per group. B: total numbers of cells were counted in BALF collected from mice treated with HDM or saline for 6 wk. Cell counts were not different between saline-treated WT mice and EGFR-M mice. HDM-treated groups all showed similar increases in total cell counts, indicating that EGFR inhibition does not alter inflammatory cell influx overall. *P < 0.05 vs. saline control group. Data were derived from 5–13 animals per group. C: cytospins, differential cell stains, and counts were performed on HDM and saline-treated groups to determine percent changes in inflammatory cell types. Macrophages were reduced similarly in all HDM-treated groups as the percentage of neutrophils and eosinophils increased; *P < 0.05 vs. saline control group; #P < 0.05 vs. WT HDM. Data were derived from 4–13 animals per group. EGFR inhibition did not alter BALF differential inflammatory cell counts with chronic HDM treatment, although increases in neutrophils in the EGFR-M mice were not as high in the other HDM-treated groups.