title: Effect of dehydroepiandrosterone on atopic dermatitis-like skin lesions induced by 1-chloro-2,4-dinitrobenzene in mouse.
abstract: BACKGROUND
  Th2 cells are overexpressed in the skin and serum of atopic dermatitis (AD) patients. Previously, we found that dehydroepiandrosterone (DHEA) decreased eosinophil infiltration in asthmatic mice through the suppression of Th2-associated cytokines. Therefore, we hypothesized that DHEA might improve the symptoms of AD syndrome.
  
  
  OBJECTIVE
  In this study, we evaluated the symptom improvement and anti-inflammatory response that result from the modulation of immunity by DHEA modulated in AD-like mice.
  
  
  METHODS
  Female BALB/c mice were sensitized and challenged with 1-chloro-2,4-dinitrobenzene. On days 14-29 after sensitization, mice were treated with cutaneous (skin smear) or oral administration of DHEA. In addition, human keratinocyte (HaCat) cells were used to evaluate the effect of DHEA on the in vitro production of proinflammatory cytokines and chemokines.
  
  
  RESULTS
  Both cutaneous and oral DHEA were able to decrease ear swelling and skin inflammation in AD-like mice. DHEA also attenuated eosinophil and mast cell infiltration into ear and skin tissue. Additionally, Th2-associated cytokines were inhibited in splenocyte culture, and suppressed the levels of IgE and interleukin 4 in serum. Oral and cutaneous administration of DHEA reduced the inflammatory response, as evidenced by AD-like skin lesions, in a similar manner. DHEA significantly reduced inflammatory cytokines and chemokines through the nuclear factor-κB and mitogen-activated protein kinases pathways in tumor necrosis factor-α activated HaCat cells.
  
  
  CONCLUSIONS
  DHEA ameliorates AD-like mouse skin inflammation and reduces eosinophil and mast cell infiltration by reducing the production of Th2-associated cytokines and chemokines.
authors.affiliation: Department of Microbiology and Immunology, Graduate Institute of Biomedical Science, Chang Gung University, 259 Wen-Hwa 1st Road, Kwei-Shan, Tao-Yuan 333, Taiwan, ROC.
authors.forename: Cheng-Chi
authors.initials: CC
authors.lastname: Chan
authors.forename: Chian-Jiun
authors.initials: CJ
authors.lastname: Liou
authors.forename: Pei-Yin
authors.initials: PY
authors.lastname: Xu
authors.forename: Jiann-Jong
authors.initials: JJ
authors.lastname: Shen
authors.forename: Ming-Ling
authors.initials: ML
authors.lastname: Kuo
authors.forename: Wen-Bin
authors.initials: WB
authors.lastname: Len
authors.forename: Liang-En
authors.initials: LE
authors.lastname: Chang
authors.forename: Wen-Chung
authors.initials: WC
authors.lastname: Huang
mesh_terms: D000276:Adjuvants, Immunologic / Q000494:pharmacology*; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology; D018925:Chemokines / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism; D003687:Dehydroepiandrosterone / Q000494:pharmacology*; D003876:Dermatitis, Atopic / Q000188:drug therapy*; D004137:Dinitrochlorobenzene / Q000494:pharmacology*; D004804:Eosinophils / Q000378:metabolism; D005260:Female; D006801:Humans; D007249:Inflammation; D015603:Keratinocytes / Q000187:drug effects; D008407:Mast Cells / Q000378:metabolism; D051379:Mice; D008807:Mice, Inbred BALB C; D010766:Phosphorylation; D012867:Skin / Q000187:drug effects*; D013154:Spleen / Q000166:cytology; D018418:Th2 Cells / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D000276:Adjuvants, Immunologic; D000893:Anti-Inflammatory Agents; D018925:Chemokines; D016207:Cytokines; D004137:Dinitrochlorobenzene; D014409:Tumor Necrosis Factor-alpha; D003687:Dehydroepiandrosterone
keywords: Atopic dermatitis; Chemokine; Cytokine; Dehydroepiandrosterone; Eosinophil