Local antimicrobial, protease and cytokine defense systems in psoriatic skin

Abstract

Background: Psoriasis vulgaris is an inflammatory skin condition characterized by dramatic biochemical and immunological changes. Aims: The aim of the study was to evaluate antimicrobial response, tissue degeneration reactions and distribution of inflammatory cytokines in untreated psoriatic skin as well as the correlations between these factors and influence on the course of the disease. Methods: We evaluated skin samples obtained from routine punch biopsies in 40 patients with psoriasis vulgaris. All tissue specimens were examined by hematoxylin and eosin staining and immunohistochemistry for human beta defensin 2 (HBD-2), matrix metalloproteinase 2 (MMP-2), tumor necrosis factor-alpha (TNF-alpha), interleukin 6 (IL-6) and IL-8. The staining intensity was semi-quantitatively graded. Results: Numerous keratinocytes, fibroblasts and macrophages expressed HBD-2 while the number of MMP-2-positive macrophages, fibroblasts and epitheliocytes varied. TNF-alpha-positive cells varied from a few to numerous in each microscopic field. IL-6-positive cells varied from a few to abundant and IL-8-positive cells from numerous to abundant in each field. Limitations: This study had a rather small patient number. Conclusions: Psoriatic skin shows a strong correlative increase in skin antimicrobial proteins and enzymes mediating tissue degeneration suggesting that the skin maintains compensatory mechanisms during persistent remodeling. While individual notable decrease in antimicrobial proteins was observed in some tissue samples, generally the increased human beta defensin associated with psoriasis is likely to be due to an altered immune status. TNF-alpha, IL-6 and IL-8 are common cytokines expressed in psoriatic skin plaques to maintain the inflammatory cycle. HBD-2, MMP-2 and TNF-alpha positively correlate with the severity of psoriasis. Meanwhile, the expression of IL-8 significantly decreases with clinically more severe psoriasis, perhaps making these factors candidate prognostic factors for psoriatic inflammation.