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Protective Effect of Botulinum Toxin Type A Against Atopic Dermatitis–Like Skin Lesions in NC/Nga Mice

Han, Sang Bum BS*,†,‡; Kim, Hyeree MD§; Cho, Sang Hyun MD, PhD§; Chung, Jin Ho MD, PhD*,†,‡; Kim, Hei Sung MD, PhD§

doi: 10.1097/DSS.0000000000001170
Original Article

BACKGROUND Botulinum neurotoxin (BTX) A possesses various biological activities, including anti-inflammatory and antipruritic actions. Human and animal studies have shown that BTX is effective in treating histamine-induced itch, lichen simplex chronicus, psoriasis, rosacea, allergic rhinitis, and scar prevention. However, its effect on atopic dermatitis (AD) has not been studied yet.

OBJECTIVE To examine the effect of BTX on AD using a mouse model. The primary outcome was skin thickness and transepidermal water loss (TEWL), and the secondary outcome was the alteration in skin severity scores, histological, and laboratory test results.

METHODS Forty-two NC/Nga mice (a mouse model for AD) were allocated into 6 groups (the untreated, 2-Chloro-1,3,5-trinitrobenzene [TNCB] alone, TNCB + BTX 30 U/kg, TNCB + BTX 60 U/kg, TNCB + vehicle [0.9% saline], TNCB + 0.03% tacrolimus). Those of the BTX group received intradermal injections of BTX on the rostral back once on the day of TNCB sensitization. The effect of BTX in TNCB-treated NC/Nga mice was assessed by measuring skin thickness, TEWL (primary outcome), the skin severity scores, histological changes of test skin including mast cell count, interleukin (IL)-4 mRNA and protein expression, and total serum IgE (secondary outcome).

RESULTS A single intradermal injection of BTX significantly suppressed skin thickness and TEWL in the TNCB-applied skin. The clinical severity scores, acanthosis and mast cell infiltration, were less in the BTX groups. BTX injection also inhibited TNCB-induced increase in IL-4 mRNA and protein expression in mice, but its effect on serum IgE level was not significant.

CONCLUSION The preliminary results suggest that BTX may be a novel approach to the prevention and supplemental treatment of acute AD lesions.

*Department of Dermatology, Seoul National University College of Medicine, Seoul, Korea;

Laboratory of Cutaneous Aging Research, Clinical Research Institute, Seoul National University Hospital, Seoul, Korea;

Institute of Dermatological Science, Seoul National University, Seoul, Korea;

§Department of Dermatology, Incheon St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Seoul, Korea

Address correspondence and reprint requests to: Hei Sung Kim, MD, PhD, Department of Dermatology, Incheon St. Mary's Hospital, The Catholic University of Korea, 56 Dongsuro, Bupyeong-gu, 150-713 Seoul, Korea, or e-mail:

Supported by a grant of the Korean Healthcare technology R&D project, Ministry of Health & Welfare, Republic of Korea (Grant No.: HN15C0105).

The authors have indicated no significant interest with commercial supporters.

S.B. Han and H. Kim contributed equally to this work.

© 2017 by the American Society for Dermatologic Surgery, Inc. Published by Wolters Kluwer Health, Inc. All rights reserved.
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