alexa Blockade of Interleukin-33 Attenuates Allergic Contact Dermatitis in Model Mice: Possible Mechanism via Eosinophil Infiltration
ISSN: 2155-9554

Journal of Clinical & Experimental Dermatology Research
Open Access

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Research Article

Blockade of Interleukin-33 Attenuates Allergic Contact Dermatitis in Model Mice: Possible Mechanism via Eosinophil Infiltration

Kazuto Taniguchi1,2*, Shuichi Yamamoto1, Emiko Hitomi1, Yukiko Inada1, Takashi Sugioka2, and Yuhei Hamasaki1

1Department of Pediatrics, Faculty of Medicine, Saga University, Japan

2Community Medical Support Institute, Faculty of Medicine, Saga University, Japan

*Corresponding Author:
Kazuto Taniguchi
Department of Pediatrics, Faculty of Medicine
Saga University, 5-1-1 Nabeshima
Saga 849-8501, Japan
Tel: +81- 952-34-2314
Fax: +81-952-34-2091
Email: taniguck@cc.saga-u.ac.jp

Received date: July 15, 2013; Accepted date: September 10, 2013; Published date: September 17, 2013

Citation: Taniguchi K, Yamamoto S, Hitomi E, Inada Y, Sugioka T, et al. (2013) Blockade of Interleukin-33 Attenuates Allergic Contact Dermatitis in Model Mice: Possible Mechanism via Eosinophil Infiltration. J Clin Exp Dermatol Res 4:183. doi: 10.4172/2155-9554.1000183

Copyright: © 2013 Taniguchi K, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

 

Abstract

Background: Interleukin (IL)-33, a novel member of the IL-1 family, is mainly produced by epithelial cells and endothelial cells. Effects of IL-33 on allergic diseases have been reported. Allergic contact dermatitis is a clinical form of contact hypersensitivity that involves a delayed-type hypersensitivity reaction. We previously reported that IL-33 is induced by tumor necrosis factor-alpha and interferon-gamma in keratinocytes and plays a critical role in allergic contact dermatitis. However, the mechanism underlying how IL-33 is involved in the pathogenesis of allergic contact dermatitis is not fully understood. We investigated the role of IL-33 in allergic contact dermatitis using model mice.

Methods: Allergic contact dermatitis model mice were generated. Epidermal thickness and eosinophil infiltration in the dermis were evaluated by histology. The function of IL-33 was investigated by in vivo administration of an anti-IL-33 antibody.

Results: Epidermal thickness was increased in the ear lesions of allergic contact dermatitis model mice. We showed that eosinophil infiltration in the dermis was increased in the ear lesions. We further found that blockade of IL- 33 attenuated not only the epidermal thickness but also the eosinophil infiltration in the dermis in the ear lesions.

Conclusions: IL-33 may promote inflammation via eosinophil infiltration in allergic contact dermatitis. Blockade of IL-33 may represent a novel and potent therapeutic strategy for allergic contact dermatitis.

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