Year: 2004
Type: article
Study design: Observational Study
Abstract: Psoriasis vulgaris is a multifactorial, chronic, inflammatory skin disease of unknown etiology. The characteristic histologic features of the disease are epidermal hyperproliferation and infiltration of both dermis and epidermis by inflammatory cells including neutrophils, lymphocytes, macrophages and mast cells. Interactions between infiltrating T cells and skin resident cells (keratinocytes, fibroblasts, endothelial cells) are often mediated by the synthesis and release of different proinflammatory cytokines1. Although the cytokine-mediated response is an essential part of the natural protective mechanism, excessive production of proinflammatory cytokines, or production of cytokines in the wrong biological context are associated with the pathology in a wide range of diseases including psoriasis. At the present time, one of the main areas of research in the psoriasis field concerns the role of cytokines in the pathogenesis of this disease. Different cytokines play a part in sustaining the two main characteristics of a psoriatic lesion; keratinocyte hyperproliferation and inflammation.1 Interleukin-2 (IL-2), interleukin-6 (IL-6), interleukin-8 (IL-8) and tumor necrosis factor-alpha (TNF-α) are the hallmark cytokines in a psoriatic cytokine network. Several investigators have suggested the possible use of TNF-α, IL-6, IL-8 and soluble interleukin-2 receptor (IL-2R) as markers of disease severity in psoriasis.2–5 Sagawa et al.6 pointed out that TNF-α in combination with other cytokines like IL-6 may be highly injurious due to complex interactions between these cytokines, suggesting a rationale for monitoring of multiple cytokines in the sera of psoriatic patients. Moreover, the cytokine assay results may vary due to the clinical stage and type of disease, methods used for cytokines detection and their sensitivities, lesion activity, interferences due to different drugs used, demographic differences in the patient groups, and the effect of concomitant pathologies.2 This preliminary study compares the serum levels of TNF-α, IL-6, IL-8 and IL-2R between 29 psoriasis patients and 25 age- and sex-matched healthy controls from the Saudi population. All the patients were untreated, both locally and systemically, for at least 14 days before enrolment. It was also ensured that control subjects had no medication during the 2 weeks before blood sampling. Blood samples (6 ml) were collected from patients and control subjects in serum separator vacutainers (BD Vacutainer Systems, Plymouth, UK). Sera were separated and immediately stored at −80 °C until analysis by commercially available enzyme-linked immunosorbent assay (ELISA) kits (R & D Systems, Minneapolis, MN). Our results showed significantly higher levels of serum cytokines in Saudi psoriasis patients as compared with healthy controls (Table 1), which is in agreement with earlier studies demonstrating a significant increase in IL-6, IL-8, IL-2R and TNF-α in sera or skin blister fluids of psoriasis patients from different ethicities.3,5,7–10 The maximal changes were observed in the levels of IL-6 (543% increase) followed by IL-8 (126%), IL-2R (77%) and TNF-α (76%). It has been suggested that proinflammatory cytokines not only play a fundamental role in the worsening of the disease or activating its pathogenetic mechanisms, but are also directly related to the clinical symptoms and disease evolution after effective therapy.2 Earlier studies have observed a significant reduction of IL-6, IL-8, IL-2R and TNF-α levels following effective therapies in psoriasis patients.2,4 We conclude that serum of proinflammatory cytokines are significantly increased in Saudi psoriasis patients, and an array of these cytokines may be considered as useful follow-up marker for monitoring of psoriatic patients and optimizing therapeutic strategies. However, detailed time-course studies on sequential analysis of these cytokines in relation to disease severity and/or treatment modalities are warranted to ascertain its real application.
Institution: Riyadh Armed Forces Hospital
Language: English
Subfield: Immunology
Field: Immunology and Microbiology
Domain: Life Sciences
Open Access status: bronze
OpenAlex ID: W2003875738