Interleukin (IL)-22, IL-17, IL-23, IL-8, vascular endothelial growth factor and tumour necrosis factor-alpha levels in patients with psoriasis before, during and after psoralen-ultraviolet A and narrowband ultraviolet B therapy
- 30 November 2010
- journal article
- research article
- Published by Oxford University Press (OUP) in British Journal of Dermatology
- Vol. 163 (6), 1282-1290
- https://doi.org/10.1111/j.1365-2133.2010.09992.x
Abstract
Background Several cross-sectional studies have shown that different cytokines and growth factors are enhanced in psoriasis. Objectives We aimed to understand the role/relation of interleukin (IL)-22, IL-17, IL-23, IL-8, vascular endothelial growth factor (VEGF) and tumour necrosis factor (TNF)-alpha in psoriasis vulgaris, addressing their levels and changes before, during and after psoralen-ultraviolet A (PUVA) and narrowband ultraviolet B (NB-UVB) treatment. Methods A cross-sectional and a longitudinal study (n = 34) - before (T0) and at 3 (T3), 6 (T6) and 12 (T12) weeks of NB-UVB and PUVA therapy - were performed; 17 patients started NB-UVB and 17 PUVA, and IL-22, IL-17, IL-23, IL-8, TNF-alpha and VEGF levels were evaluated. Results At T0, compared with controls (n = 20), all the parameters were significantly higher in patients, except for TNF-alpha. Both NB-UVB and PUVA treatment gave, at T3, a significant decrease in TNF-alpha and IL 23; IL 22 and IL 17 decreased significantly at T6; all parameters and Psoriasis Area and Severity Index decreased significantly at T12. However, in both groups, at T12, VEGF was still significantly higher than control. Conclusions Psoriasis seems to be a complex disease in which the cytokine network is disturbed, namely in levels of IL-22, IL-17, IL-23, IL-8, TNF-alpha and VEGF. NB-UVB and PUVA follow-up studies suggested that the reduction in the IL-23/Th17 axis might be important in the pathogenic mechanisms of psoriasis. Further follow-up studies of patients with psoriasis treated with these and other therapies could be very helpful for the understanding of the disturbance in the cytokine network in psoriasis and indirectly in its pathogenesis.Keywords
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