Dihomo-gamma-linolenic acid prevents the development of atopic dermatitis through prostaglandin D-1 production in NC/Tnd mice

作者：Amagai Yosuke; Oida Kumiko; Matsuda Akira; Jung Kyungsook; Kakutani Said; Tanaka Takao; Matsuda Kenshiro; Jang Hyosun; Ahn Ginae; Xia Yan; Kawashima Hiroshi; Shibata Hiroshi; Matsuda Hiroshi^*; Tanaka Akane

来源：Journal of Dermatological Science, 2015, 79(1): 30-37.

DOI：10.1016/j.jdermsci.2015.03.010

• Atopic dermatitis
• Dihomo-gamma-linolenic acid
• Prostaglandin D-1
• NC/Tnd mouse

Background: Atopic dermatitis (AD) is a chronic and relapsing skin disorder with pruritic skin symptoms. We previously reported that dihomo-gamma-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 D-1 (PGD(1)) was measured. Furthermore, effect of PGD(1) 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 PGD(1), which correlated with a better outcome in NC/Tnd mice. Moreover, we confirmed that mast cells produced PGD(1) after DGLA exposure, thereby exerting a suppressive effect on immunoglobulin E-mediated degranulation. PGD(1) 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/Td mice by regulating the PGD(1) supply.

• 出版日期2015-7