Department of Medicine, Dermatology and Venereology Unit, Karolinska University Hospital, Solna, Karolinska Institutet, Stockholm, Sweden.
Br J Dermatol. 2011 May;164(5):1023-9. doi: 10.1111/j.1365-2133.2011.10241.x.
BACKGROUND Various mediators of pruritus have been suggested that might be responsible for the mechanism of pruritus in psoriasis.
To study the expression levels of members of the tachykinin family, substance P and neurokinin (NK) A and their receptors, NK-1 and NK-2, in psoriasis and to correlate their expression with the intensity of pruritus. A possible correlation with chronic stress and depression was also evaluated.
Biopsies were obtained from 28 patients with chronic plaque psoriasis; the majority had pruritus. The samples were taken from lesional and nonlesional areas on the back and also from 10 healthy controls, for immunohistochemistry staining, and from lesional skin for radioimmunoassay. Prior to biopsy, the clinical severity of the psoriasis of each patient was assessed by the Psoriasis Area and Severity Index (PASI) and the intensity of pruritus was measured by using a visual analogue scale (VAS). Levels of depression and stress were measured using Beck's Depression Inventory (BDI) and the salivary cortisol test, respectively.
Substance P-, NKA- and NK-2 receptor-immunoreactive nerves, and non-neuronal inflammatory cells positive for substance P and NKA and their respective receptors, NK-1 and NK-2, were numerous in psoriasis compared with healthy controls. The numbers of substance P-positive nerves and NK-2 receptor-positive cells in lesional skin were significantly correlated to pruritus intensity. The cortisol ratio was inversely correlated with the number of NK-1 receptor-immunoreactive inflammatory cells in lesional and nonlesional psoriasis skin. There was also a positive correlation between the BDI score and the number of substance P-positive cells in nonlesional skin and with NK-1 receptor-positive cells in lesional and nonlesional skin.
Tachykinins may play a role in psoriasis per se, in addition to pruritus in this disease. Targeting the combined NK-1 and NK-2 receptors might be a possible treatment.
研究速激肽家族成员、P 物质和神经激肽（NK）A 及其受体 NK-1 和 NK-2 在银屑病中的表达水平，并将其与瘙痒强度相关联。还评估了与慢性应激和抑郁的可能相关性。
从 28 例慢性斑块状银屑病患者中获取活检样本；大多数患者有瘙痒。将样本取自背部的病变和非病变区域，还取自 10 例健康对照者，用于免疫组织化学染色，并取自病变皮肤进行放射免疫测定。在活检之前，使用银屑病面积和严重程度指数（PASI）评估每位患者的银屑病临床严重程度，并用视觉模拟量表（VAS）测量瘙痒强度。使用贝克抑郁量表（BDI）和唾液皮质醇测试分别测量抑郁和应激水平。
与健康对照组相比，银屑病中 P 物质、NKA 和 NK-2 受体免疫反应性神经以及 P 物质和 NKA 阳性的非神经炎症细胞及其各自的受体 NK-1 和 NK-2 数量众多。病变皮肤中 P 物质阳性神经和 NK-2 受体阳性细胞的数量与瘙痒强度显著相关。皮质醇比值与病变和非病变银屑病皮肤中 NK-1 受体免疫反应性炎症细胞的数量呈负相关。BDI 评分与非病变皮肤中 P 物质阳性细胞的数量以及病变和非病变皮肤中 NK-1 受体阳性细胞的数量呈正相关。
除了这种疾病的瘙痒外，速激肽可能在银屑病本身中起作用。靶向联合的 NK-1 和 NK-2 受体可能是一种可能的治疗方法。
