title: Prolactin induces the production of Th17 and Th1 cytokines/chemokines in murine Imiquimod-induced psoriasiform skin.
abstract: BACKGROUND
  Prolactin (PRL) is a pituitary-derived neuropeptide hormone that has been suggested to promote the development of psoriasis, a Th17/Th1-mediated inflammatory dermatosis. PRL increases the expression of Th1 cytokines; however, its effects on Th17 responses are unknown.
  
  
  OBJECTIVE
  This study aims to determine the in vivo effects of PRL on the expression of Th17 cytokines/chemokines in imiquimod-induced psoriasiform skin inflammation in mice.
  
  
  METHODS
  BALB/c mice were intraperitoneally injected with PRL or phosphate-buffered saline, and imiquimod cream or Vaseline was applied to the shaved back skin for six consecutive days.
  
  
  RESULTS
  Intraperitoneal PRL increased the mRNA levels of IL-17A, IL-17F, IL-22, IL-23p19, IL-12p40, CCL20 and STAT3 in imiquimod-treated skin. Mice treated with imiquimod plus PRL, but not those treated with imiquimod plus phosphate-buffered saline, showed significantly increased mRNA levels of TNF-α, IFN-γ, IL-12p35 and CXCL2 compared with controls. Intraperitoneal PRL increased the numbers of CD3(+) and GR-1(+) cells in the dermis of imiquimod-treated skin.
  
  
  CONCLUSIONS
  These results suggest that intraperitoneal PRL enhances the expression of Th17 and Th1 cytokines/chemokines, and augments inflammation in imiquimod-induced psoriasiform skin. Prolactin may thus exacerbate psoriasis through the enhancement of Th17/Th1 responses.
authors.affiliation: Department of Dermatology, Teikyo University School of Medicine, Tokyo, Japan; Department of Dermatology, Faculty of Medicine, University of Tokyo, Tokyo, Japan.
authors.forename: C S
authors.initials: CS
authors.lastname: Hau
authors.forename: N
authors.initials: N
authors.lastname: Kanda
authors.forename: Y
authors.initials: Y
authors.lastname: Tada
authors.forename: S
authors.initials: S
authors.lastname: Shibata
authors.forename: S
authors.initials: S
authors.lastname: Sato
authors.forename: S
authors.initials: S
authors.lastname: Watanabe
mesh_terms: D000634:Aminoquinolines / Q000633:toxicity; D000818:Animals; D016207:Cytokines / Q000235:genetics*; D004195:Disease Models, Animal; D005260:Female; D000077271:Imiquimod; D007274:Injections, Intraperitoneal; D051379:Mice; D008807:Mice, Inbred BALB C; D011388:Prolactin / Q000627:therapeutic use*; D011565:Psoriasis / Q000139:chemically induced / Q000188:drug therapy* / Q000276:immunology; D012333:RNA, Messenger / Q000235:genetics; D060888:Real-Time Polymerase Chain Reaction; D011994:Recombinant Proteins; D018417:Th1 Cells / Q000276:immunology*; D058504:Th17 Cells / Q000276:immunology*
chemical_list: D000634:Aminoquinolines; D016207:Cytokines; D012333:RNA, Messenger; D011994:Recombinant Proteins; D011388:Prolactin; D000077271:Imiquimod