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Possible role of Malassezia furfur in psoriasis: modulation of TGF‐β1, integrin, and HSP70 expression in human keratinocytes and in the skin of psoriasis‐affected patients
Author(s) -
Baroni Adone,
Paoletti Iole,
Ruocco Eleonora,
Agozzino Marina,
Tufano Maria Antonietta,
Donnarumma Giovanna
Publication year - 2004
Publication title -
journal of cutaneous pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.597
H-Index - 75
eISSN - 1600-0560
pISSN - 0303-6987
DOI - 10.1046/j.0303-6987.2004.0135.x
Subject(s) - psoriasis , pathogenesis , keratinocyte , signal transduction , human skin , integrin , cancer research , biology , immunology , medicine , pathology , cell , microbiology and biotechnology , cell culture , biochemistry , genetics
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. Materials and 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‐β1 (TGF‐β1), 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‐β1, integrin chains, and HSP70 expression was found. Conclusion: Our data suggest that M. furfur can induce the overproduction of molecules involved in cell migration and hyperproliferation, thereby favoring the exacerbation of psoriasis.