Funding sources The study was supported by the Swedish Psoriasis Association, the Welander/Finsen Foundation and the Karolinska Institutet.
CLINICAL AND LABORATORY INVESTIGATIONS
Expression of tachykinins and their receptors in plaque psoriasis with pruritus
Article first published online: 26 APR 2011
© 2011 The Authors. BJD © 2011 British Association of Dermatologists
British Journal of Dermatology
Volume 164, Issue 5, pages 1023–1029, May 2011
How to Cite
Amatya, B., El-Nour, H., Holst, M., Theodorsson, E. and Nordlind, K. (2011), Expression of tachykinins and their receptors in plaque psoriasis with pruritus. British Journal of Dermatology, 164: 1023–1029. doi: 10.1111/j.1365-2133.2011.10241.x
Conflicts of interest M.H. is a full time contractor with Pfizer Inc.
- Issue published online: 26 APR 2011
- Article first published online: 26 APR 2011
- Accepted manuscript online: 7 FEB 2011 09:25AM EST
- Accepted for publication 25 January 2011
Background Various mediators of pruritus have been suggested that might be responsible for the mechanism of pruritus in psoriasis.
Objectives 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.
Methods 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.
Results 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.
Conclusions 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.