Bakry Ola Ahmed, Samaka Rehab Monir, Shoeib Mohamed Abdel Moneim, Abdel Aal Sara Mohamed
Department of Dermatology, Andrology and STDs, Faculty of Medicine, Menoufiya University , Shibeen El Koom , Egypt and.
Ultrastruct Pathol. 2015 Feb;39(1):49-61. doi: 10.3109/01913123.2014.952470. Epub 2014 Sep 12.
Nuclear factor kappa B (NFκB) is a key regulatory element in a variety of immune and inflammatory pathways, cellular proliferation, differentiation and apoptosis. Cyclo-oxygenase 2 (COX2) is one of the downstream targets of NFκB. The current work aimed to explore the possible role of NFκB and COX2 in psoriasis pathogenesis through their immunohistochemical (IHC) expression in skin biopsies of this disease and correlating this expression with clinico-pathological parameters of studied cases. 103 subjects were studied; including 58 cases with psoriasis vulgaris (lesional and perilesional skin) and 45 normal, age- and gender-matched subjects, as a control group. NFκB and COX2 expressions were evaluated using standard IHC techniques. NFκB and COX2 were upregulated in psoriasis lesional skin compared to perilesional (p < 0.001 for both) and control skin (p < 0.001 for both). Higher NFκB and COX2 H scores were significantly associated with absent granular cell layer (p = 0.02 for both), severe degree of perivascular inflammatory infiltrate (p = 0.03 and 0.002, respectively) and thin suprapapillary epidermis (p = 0.003 and 0.006, respectively). Significant positive correlation was noted between NFκB and COX2 H scores in epidermis (r = 0.41, p = 0.02) and dermis (r = 0.6, p = 0.04) of lesional skin. Significant positive correlation between NFκB H score and PASI score (r = 0.38, p = 0.04) and between COX2 H score and PASI score (r = 0.52, p < 0.001) were detected in lesional epidermis. In conclusion, both NFκB and COX2 play a role in the pathogenesis of chronic plaque psoriasis. This may open an avenue for research for new therapeutic modalities based on their inhibition.
核因子κB(NFκB)是多种免疫和炎症途径、细胞增殖、分化及凋亡中的关键调节因子。环氧化酶2(COX2)是NFκB的下游靶点之一。当前研究旨在通过检测核因子κB(NFκB)和环氧化酶2(COX2)在银屑病皮肤活检组织中的免疫组化(IHC)表达,并将其与研究病例的临床病理参数相关联,来探讨它们在银屑病发病机制中的可能作用。本研究共纳入103名受试者,其中包括58例寻常型银屑病患者(皮损及皮损周边皮肤)和45名年龄及性别匹配的正常受试者作为对照组。采用标准免疫组化技术评估NFκB和COX2的表达。与皮损周边皮肤(两者p均<0.001)及对照皮肤(两者p均<0.001)相比,银屑病皮损皮肤中NFκB和COX2表达上调。较高的NFκB和COX2 H评分与颗粒细胞层缺失(两者p均=0.02)、血管周围炎症浸润严重程度(分别为p=0.03和0.002)及乳头上方表皮变薄(分别为p=0.003和0.006)显著相关。在皮损皮肤的表皮(r=0.41,p=0.02)和真皮(r=0.6,p=0.04)中,NFκB和COX2 H评分之间存在显著正相关。在皮损表皮中检测到NFκB H评分与银屑病面积和严重程度指数(PASI)评分之间存在显著正相关(r=0.38,p=0.04),以及COX2 H评分与PASI评分之间存在显著正相关(r=0.52,p<0.001)。总之,NFκB和COX2均在慢性斑块状银屑病的发病机制中发挥作用。这可能为基于对它们的抑制作用的新治疗方式研究开辟一条途径。