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Protective Effect of Botulinum Toxin Type A Against Atopic Dermatitis-Like Skin Lesions in NC/Nga Mice
Sang Bum Han1, Hyeree Kim, Sang Hyun Cho
1*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.
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.
