2. Academic Validation
  3. Dihomo-γ-linolenic acid prevents the development of atopic dermatitis through prostaglandin D1 production in NC/Tnd mice

Dihomo-γ-linolenic acid prevents the development of atopic dermatitis through prostaglandin D1 production in NC/Tnd mice

  • J Dermatol Sci. 2015 Jul;79(1):30-7. doi: 10.1016/j.jdermsci.2015.03.010.
Yosuke Amagai 1,  Kumiko Oida 1,  Akira Matsuda 2,  Kyungsook Jung 3,  Saki Kakutani 4,  Takao Tanaka 4,  Kenshiro Matsuda 1,  Hyosun Jang 1,  Ginae Ahn 1,  Yan Xia 1,  Hiroshi Kawashima 4,  Hiroshi Shibata 4,  Hiroshi Matsuda 5,  Akane Tanaka 6
Affiliations

Affiliations

  • 1 Cooperative Major in Advanced Health Science, Graduate School of Bio-Applications and System Engineering, Tokyo University of Agriculture and Technology, Tokyo, Japan.
  • 2 Laboratory of Veterinary Molecular Pathology and Therapeutics, Division of Animal Life Science, Institute of Agriculture, Tokyo, Japan.
  • 3 Laboratory of Comparative Animal Medicine, Division of Animal Life Science, Institute of Agriculture, Tokyo University of Agriculture and Technology, Tokyo, Japan.
  • 4 Institute for Health Care Science, Suntory Wellness Ltd., Osaka, Japan.
  • 5 Cooperative Major in Advanced Health Science, Graduate School of Bio-Applications and System Engineering, Tokyo University of Agriculture and Technology, Tokyo, Japan; Laboratory of Veterinary Molecular Pathology and Therapeutics, Division of Animal Life Science, Institute of Agriculture, Tokyo, Japan. Electronic address: hiro@cc.tuat.ac.jp.
  • 6 Cooperative Major in Advanced Health Science, Graduate School of Bio-Applications and System Engineering, Tokyo University of Agriculture and Technology, Tokyo, Japan; Laboratory of Comparative Animal Medicine, Division of Animal Life Science, Institute of Agriculture, Tokyo University of Agriculture and Technology, Tokyo, Japan. Electronic address: akane@cc.tuat.ac.jp.
PMID: 25907057 DOI: 10.1016/j.jdermsci.2015.03.010
Abstract

Background: Atopic dermatitis (AD) is a chronic and relapsing skin disorder with pruritic skin symptoms. We previously reported that dihomo-γ-linolenic acid (DGLA) prevented the development of AD in NC/Tnd mice, though the mechanism remained unclear.

Objective: We attempted to investigate the mechanism of preventive effect of DGLA on AD development in NC/Tnd mice.

Methods: The clinical outcomes of NC/Tnd mice that were given diets containing DGLA, arachidonic acid, or eicosapentaenoic acid were compared. Lipid mediator contents in the skin in each group were also quantified. In addition, release of lipid mediators from RBL-2H3 mast cells treated with either DGLA or prostaglandin D1 (PGD1) was measured. Furthermore, effect of PGD1 on gene expression of thymic stromal lymphopoietin (TSLP) in PAM212 keratinocyte cells was determined.

Results: Only DGLA containing diet suppressed the development of dermatitis in vivo. By quantifying the 20-carbon fatty acid-derived eicosanoids in the skin, the application of DGLA was found to upregulate PGD1, which correlated with a better outcome in NC/Tnd mice. Moreover, we confirmed that mast cells produced PGD1 after DGLA exposure, thereby exerting a suppressive effect on immunoglobulin E-mediated degranulation. PGD1 also suppressed gene expression of TSLP in keratinocytes.

Conclusion: These results suggest that oral administration of DGLA causes preventive effects on AD development in NC/Tnd mice by regulating the PGD1 supply.

Keywords

Atopic dermatitis; Dihomo-γ-linolenic acid; NC/Tnd mouse; Prostaglandin D(1).

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