Biomolecules & Therapeutics  https://doi.org/10.4062/biomolther.2020.036
Topical Application of S1P2 Antagonist JTE-013 Attenuates 2,4-Dinitrochlorobenzene-Induced Atopic Dermatitis in Mice
Jisoo Kang1, Ju-Hyun Lee2 and Dong-Soon Im1,2,*
1Laboratory of Pharmacology, College of Pharmacy, Pusan National University, Busan 46241,
2Laboratory of Pharmacology, College of Pharmacy, and Department of Life and Nanopharmaceutical Sciences, Graduate School, Kyung Hee University, Seoul 02447, Republic of Korea
*E-mail: imds@khu.ac.kr
Tel: +82-2-961-9377, Fax: +82-2-961-9580
Received: March 6, 2020; Revised: April 10, 2020; Accepted: April 29, 2020; Published online: June 3, 2020.
© The Korean Society of Applied Pharmacology. All rights reserved.

Abstract
Sphingosine-1-phosphate (S1P) and its receptors have been implicated in atopic dermatitis. S1P2 was found to function as a proallergic receptor, while its antagonist JTE-013 was found to suppress allergic asthma in mice. Topical application of JTE-013 has not been investigated in an in vivo model of atopic dermatitis. Therefore, the therapeutic potential of JTE-013 topical application was evaluated by the use of a 2,4-dinitrochlorobenzene (DNCB)-induced atopic dermatitis mouse model. DNCB-induced inflammation and mast cell accumulation in skin tissues were significantly suppressed by topical JTE-013 treatment in BALB/c mice. DNCB-induced increase of lymph nodes sizes and elevated inflammatory cytokines (IL-4, IL-13, IL-17, and IFN-γ) in lymph nodes were also significantly reduced by the JTE-013 treatment. Elevated serum levels of IgE were significantly suppressed through the topical treatment of JTE-013. In summary, the topical treatment of JTE-013 S1P2 antagonist suppressed DNCB-induced atopic dermatitis symptoms and immune responses. These results suggested JTE-013 as a potential therapeutic agent for atopic dermatitis.
Keywords: Atopy, Dermatitis, Dendritic cell, Sphingosine 1-phosphate, S1P2


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