title: Possible role of Malassezia furfur in psoriasis: modulation of TGF-beta1, integrin, and HSP70 expression in human keratinocytes and in the skin of psoriasis-affected patients.
abstract: BACKGROUND
  Psoriasis is a disease characterized by an abnormal pattern of keratinocyte growth and differentiation. Malassezia furfur forms part of the normal human skin flora. It may also be involved in the pathogenesis of psoriasis. To define the role of M. furfur in the pathogenesis of psoriasis, we investigated how M. furfur regulates molecules involved in cell migration and proliferation. The experiments were performed using human keratinocytes and skin biopsies from M. furfur-positive and -negative psoriasis-affected patients. In addition, we examined the signal transduction mechanisms involved.
  
  
  METHODS
  Western blot analysis was performed on human keratinocytes lysates treated or untreated with M. furfur and on biopsies from healthy and psoriasis patients. Signal transduction mechanisms involved were evaluated by electrophoretic mobility shift assay using the AP-1 inhibitor curcumin.
  
  
  RESULTS
  We found that M. furfur up-regulates transforming growth factor-beta1 (TGF-beta1), integrin chain, and HSP70 expression in human keratinocytes via AP-1-dependent mechanism. In the biopsies of M. furfur-positive psoriasis-affected patients, an increase in TGF-beta1, integrin chains, and HSP70 expression was found.
  
  
  CONCLUSIONS
  Our data suggest that M. furfur can induce the overproduction of molecules involved in cell migration and hyperproliferation, thereby favoring the exacerbation of psoriasis.
authors.affiliation: Department of Dermatology, Second University of Naples, Via Constantinopoli 16, 80138 Naples, Italy.
authors.forename: Adone
authors.initials: A
authors.lastname: Baroni
authors.forename: Iole
authors.initials: I
authors.lastname: Paoletti
authors.forename: Eleonora
authors.initials: E
authors.lastname: Ruocco
authors.forename: Marina
authors.initials: M
authors.lastname: Agozzino
authors.forename: Maria Antonietta
authors.initials: MA
authors.lastname: Tufano
authors.forename: Giovanna
authors.initials: G
authors.lastname: Donnarumma
mesh_terms: D015153:Blotting, Western; D002455:Cell Division / Q000502:physiology; D002465:Cell Movement / Q000502:physiology; D002478:Cells, Cultured; D018840:HSP70 Heat-Shock Proteins / Q000378:metabolism*; D006801:Humans; D016023:Integrins / Q000378:metabolism*; D015603:Keratinocytes / Q000378:metabolism / Q000382:microbiology* / Q000473:pathology; D008290:Malassezia / Q000472:pathogenicity* / Q000502:physiology; D011565:Psoriasis / Q000378:metabolism / Q000382:microbiology* / Q000473:pathology; D015398:Signal Transduction; D012867:Skin / Q000378:metabolism / Q000382:microbiology* / Q000473:pathology; D018808:Transcription Factor AP-1 / Q000502:physiology; D016212:Transforming Growth Factor beta / Q000378:metabolism*; D053773:Transforming Growth Factor beta1
chemical_list: D018840:HSP70 Heat-Shock Proteins; D016023:Integrins; C508960:TGFB1 protein, human; D018808:Transcription Factor AP-1; D016212:Transforming Growth Factor beta; D053773:Transforming Growth Factor beta1