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-kB) 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-kB 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-kB. 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 ¼ 0.0001). Nuclear expression of NF-kB was detected in 66% of psoriatic lesions; this active phosphorylated form was significantly over expressed in psoriasis in comparison with normal skin (p ¼ 0.0004). Diffuse nuclear expression of NF-kB was significantly associated with up-regulation of survivin in psoriatic plaque (p ¼ 0.03). Conclusions: Survivin and NF-kB appeared to be important factors in the pathogenesis of psoriasis. Survivin could be the target of NF-kB mediating its death signal inhibition pathway in psoriasis.Abdou AG, Hanout HM. Evaluation of survivin and NF-kB in psoriasis, an immunohistochemical study.

Background S100A8 single nucleotide polymorphism (SNP) and S100A8 blood level are related to many inflammatory disorders with no available conclusion in psoriasis. Aim The aim of this study was to evaluate the possible role of S100A8 in psoriasis pathogenesis through analyzing its S100A8 (rs3806232) gene polymorphism and S100A8 serum level in psoriasis vulgaris patients, in addition to correlate the detected results with severity psoriasis in those patients. Methods This case–control study was conducted on 50 patients having psoriasis vulgaris, and 26 controls. Severity of psoriasis was evaluated using psoriasis area and severity index (PASI) score. S100A8 serum level and S100A8 (rs3806232) SNP were evaluated by ELISA and polymerase chain reaction‐restriction fragment length polymorphism (PCR‐RFLP) respectively. Results Serum S100A8 level was significantly higher in psoriatic patients than controls and was positively correlated with PASI score (r = 0.826, p < 0.001). S100A8 (rs3806232) AA genotype and A allele were significantly increased among psoriasis patients than controls (p < 0.001) increasing risk of psoriasis development by about 5, 12, and 6 times than AG, GG, and G alleles. AA genotype was significantly associated with psoriasis severity (p = 0.005) and high S100A8 serum levels (p = 0.018). Conclusions Circulating S100A8 could associated with disease severity and have an active role in psoriasis pathogenesis. S100A8 (rs3806232) SNP (AA genotype and A allele) might contribute to development and severity of psoriasis in the Egyptian population.

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