title: Topical application of PPARα (but not β/δ or γ) suppresses atopic dermatitis in NC/Nga mice.
abstract: BACKGROUND
  Peroxisome proliferator-activated receptors (PPARs) are nuclear receptors, which regulate not only adipogenesis and proliferation/differentiation but also the immune response of cells. Because topical application of the activators of some PPAR isoforms improved clinical symptoms in patients with atopic dermatitis (AD), we investigated the role of PPAR activators using a murine AD model in NC/Nga mice; to the best of our knowledge, this has not been previously reported.
  
  
  METHODS
  Activators of three PPAR isoforms (α, β/δ, γ) were topically applied on inflamed skin in a murine AD model that was developed by repeated topical application of mite antigen in NC/Nga mice. The efficacy of each topical PPAR activator was evaluated immunologically and serologically.
  
  
  RESULTS
  Topical application of the PPARα activator, but not of the activators of PPARβ/δ or PPARγ, improved clinical dermatitis, reduced inflammatory cell infiltration in the dermis, and alleviated the elevation of serum IgE levels. In addition, PPARα expression was downregulated in the epidermis in our murine AD model, as is seen in patients with AD.
  
  
  CONCLUSIONS
  Topical application of PPARα activator could be a potent therapeutic agent for patients with AD and could take the place of topical steroid treatments.
authors.affiliation: Department of Dermatology, School of Medicine, Kyushu University, Fukuoka, Japan. allheartakita@yahoo.co.jp
authors.forename: T
authors.initials: T
authors.lastname: Chiba
authors.forename: S
authors.initials: S
authors.lastname: Takeuchi
authors.forename: H
authors.initials: H
authors.lastname: Esaki
authors.forename: K
authors.initials: K
authors.lastname: Yamamura
authors.forename: Y
authors.initials: Y
authors.lastname: Kurihara
authors.forename: Y
authors.initials: Y
authors.lastname: Moroi
authors.forename: M
authors.initials: M
authors.lastname: Furue
mesh_terms: D000818:Animals; D003876:Dermatitis, Atopic / Q000188:drug therapy* / Q000276:immunology / Q000473:pathology; D004195:Disease Models, Animal; D004804:Eosinophils / Q000166:cytology; D004817:Epidermis / Q000276:immunology / Q000378:metabolism; D005260:Female; D007073:Immunoglobulin E / Q000097:blood / Q000276:immunology; D008407:Mast Cells / Q000166:cytology; D051379:Mice; D047493:PPAR alpha / Q000819:agonists* / Q000378:metabolism; D011743:Pyrimidines / Q000008:administration & dosage / Q000494:pharmacology
chemical_list: D047493:PPAR alpha; D011743:Pyrimidines; D007073:Immunoglobulin E; C006253:pirinixic acid