Severe cases of poison ivy, oak, or sumac-induced allergic contact dermatitis (ACD) is a major health hazard especially when affecting the lungs, eyes, or large proportions of skin. Urushiol is the major active ingredient of poison ivy which is believed to mediate the intense allergic skin reactions. However, no robust preclinical models exist to assess the effectiveness of new agents in ACD. In the present experiment, we established a protocol in mice for reproducible induction of dermatitis by the poison ivy active ingredient, urushiol. Also, using flow-cytometry and qRT-PCR, we identified that Th17-derived cytokines underlie poison ivy-induced skin reactions. Animals were first sensitized with urushiol by application on shaved abdominal skin. Afterwards, animals received several challenges with urushiol by application on both ears. Ear thickness was measured with a micrometer and redness was scored visually.
Concentration-response experiments using different dose levels of urushiol for sensitization and subsequent challenges showed that sensitization with 2% urushiol and at least 5 subsequent challenges with 1% urushiol are required for optimal induction of the ACD. In flow-cytometry experiments, Th17 cells were found to be the major subset that is increased following ACD induction. In qRT-PCR experiments, we found that genes for IL-17A, IL-17F and IL-22 were increased in the ear following urushiol ACD induction. Steroidal drugs clobetasol and dexamethasone alleviated urushiol-induced ACD in the mice.