Relationship between TRPV1-GRPR-JAK1STAT3 pathway expression and pruritus in allergic contact dermatitis
TIAN Limin, YANG Sen, LI Wei, A Surui, HUYAN Xiaohui, YANG Yuenan
Department of Dermatology and Venereology, The First Affiliated Hospital of Baotou Medical College, Inner Mongolia University of Science and Technology, Baotou 014010, China
Abstract：Objective To investigate Transient receptor potential (TRPV1) - Gastrin releasing peptide receptor, GRPR) -JAK1STAT3 signaling mechanism on skin pruritus in allergic contact dermatitis. Methods The allergic contact dermatitis (ACD) model was induced by dibutyl cubic acid (SADBE) in mice, which were divided into normal group, SADBE group and TRPV1 knockout group. Detect skin thickness and serum immunoglobulin E (IgE). Immunofluorescence and FISH staining were used to detect the expression of Keratin (KRT14), TRPV1 and GRPR in antibody cells, analyze the correlation between their expression and the number of scratches in mice, and fluorescence quantitative polymerase chain reaction (qPCR) was used to detect the expression of TRPV1-GRPR-JAK1STAT3 signal in the spinal cord of ACD model mice. Results In the mouse ACD model induced by SADBE, prolonged skin itching was observed between 3 and 7 days. Elevated serum IgE levels, thickened epidermis, and increased spleen weight were observed also. Dual FISH studies of lumbar spinal cord sections in mice showed significant overlap between TRPV1 and GRPR, with increased expression of TRPV1, GRPR, JAK1, and STAT3 mRNA in the SADVE group compared with the normal group and decreased expression in the SADBE group after TRPV1 knockout. The number of scratches and epidermal thickness decreased in TRPV1 knockout group, and the difference was statistically significant (P<0.05). Conclusion ACD induced by SADBE resulted in increased pruritus in mice, while inhibition of TRPV1-GRPR-JAK1STAT3 signaling suppressed allergic contact dermatitis skin pruritus.
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2023, Vol. 20 
