Establishment of a Nail Psoriasis Mouse Model by Topical Application of Imiquimod After Nail Removal.

Abstract

The chronic and intractable nature of nail psoriasis affects patients' QOL physically and psychologically. There is a need for the development of more effective treatments with fewer side effects. The establishment of a simple mouse model of nail psoriasis would facilitate the development of new treatments for nail psoriasis. Application of imiquimod on mouse skin can induce psoriasis-like skin inflammation, and it is now widely used as a psoriasis mouse model. We hypothesized that imiquimod application on the nail beds and surrounding areas would induce the formation of inflamed nail lesions and could serve as a model of nail psoriasis. Mice treated topically with imiquimod for 7 days with nail removal showed nail lesions that macroscopically and histopathologically resembled human nail psoriasis. Immunohistochemistry analysis showed elevated expression levels of epidermal differentiation and proliferation markers and their transcription factor (CK6, CK10, NF-κB), increased inflammatory cell infiltration (CD3, CD4, Gr-1), and decreased expression of an anti-inflammatory mediator (IL-10). In mice digits treated topically with imiquimod for 7 days with nail removal, the gene expression of IL-17A/F was upregulated in qPCR. The results suggest the similarity between imiquimod-induced nail lesions and human nail psoriasis. Our results suggest that this model has the potential to allow fast therapeutic screenings, promote nail psoriasis research, and facilitate the development of new treatments for nail psoriasis.