Evaluation of survivin and NF-kappaB in psoriasis, an immunohistochemical study

Abstract

Background: Suppression of apoptosis is generally one of the accepted pathogenetic mechanisms for psoriasis and any epidermal hyperproliferative states. Survivin is a member of the inhibitor of apoptosis protein family mediating its apoptosis suppressive function by the inhibition of caspase pathway. Nuclear factor kappa B (NF-kappaB) is a transcription factor that regulates hundreds of genes including many critically involved in apoptosis. The aim of this study was to explore the role could be played by survivin and NF-kappaB in psoriasis and the link between them.

Methods: Thirty cases of lesional psoriasis, 10 perilesional and 10 control specimens from normal skin were studied by immunohistochemical method for expression of survivin and NF-kappaB.

Results: Survivin was detected in 73% of psoriatic lesions distributed either in epidermis, in endothelial cells of proliferating capillaries or in both of them. In non-psoriatic lesions either perilesional or control specimens, survivin was confined to basal layer of epidermis, significantly up regulated in psoriasis in comparison with non-psoriatic lesions (p = 0.0001). Nuclear expression of NF-kappaB was detected in 66% of psoriatic lesions; this active phosphorylated form was significantly over expressed in psoriasis in comparison with normal skin (p = 0.0004). Diffuse nuclear expression of NF-kappaB was significantly associated with up-regulation of survivin in psoriatic plaque (p = 0.03).

Conclusions: Survivin and NF-kappaB appeared to be important factors in the pathogenesis of psoriasis. Survivin could be the target of NF-kappaB mediating its death signal inhibition pathway in psoriasis.