Epidemiologic studies have suggested that the skin is an early entry point for antigen sensitization as suggested by the frequent occurrence of allergic dermatitis (AD) prior to the development of allergic disorders. We therefore hypothesized that epicutaneous antigen exposure would prime for airway and esophageal allergic responses in an experimental model.

AD was induced by applying 100 micrograms of Aspergillus Fumigatus antigen or Vehicle soaked patches on the shaved back of BALB/c mice, at two one week intervals over the course of four weeks. To establish airway and esophageal inflammation, we examined respiratory hyperresponsiveness to methacholine and inflammation in the bone marrow, skin, airways and esophagus.

Significant skin symptoms including lichenification and excoriations developed in the antigen-sensitized group, whereas no cutaneous changes were observed in the vehicle group (P<0.001). We also observed increases in immunological responses in the antigen-sensitized group: 1062 ± 178ng/ml of total IgE, 1215 ± 375×10 dilution-titer at OD0.09 of antigen-specific IgG1, 28.5 ± 23.4×10⁴cells/ml of blood eosinophils, whereas in the vehicle group: 372.8 ± 127.3, 2.8 ± 0.3, 11.4 ± 9.5, respectively (mean ± SEM, p<0.01). Furthermore, an intranasal antigen challenge induced nasal and airway hyperresponsiveness (p<0.01) and eosinophilia in the airway and esophagus. The eosinophils in the broncho-alveolar lavage fluid (BALF) were 35.8 ± 9.9×10⁴cells/ml and 28.1 ± 6.5cells/mm² in the esophagus, whereas 3.1 ± 1.7 and 4.9 ± 1.4 in the vehicle controls (p<0.01 and p<0.05, respectively).

Epicutaneous antigen sensitization followed by a single airway antigen challenge induces systemic responses in the respiratory tract and esophagus. These results highlight the potency of epicutaneous antigen exposure in the development of allergic responses.