Open Access

ARTICLE

Proinflammatory cytokine responses in patients with psoriasis

Anargyros Kouris¹, Aikaterini Pistiki², Alexandros Katoulis¹, Marianna Georgitsi², Sofia Giatrakou¹, Evangelia Papadavid¹, Mihai G. Netea³, Nikolaos Stavrianeas¹, Evangelos J. Giamarellos-Bourboulis^2,3

1 2^nd Department of Dermatology and Venereology, National and Kapodistrian University of Athens, Medical School, Athens, Greece
2 4^th Department of Internal Medicine, National and Kapodistrian University of Athens, Medical School, Athens, Greece
3 Department of Medicine and Nijmegen Institute for Infection, Inflammation and Immunity, Radboud University Nijmegen Medical Centre,TheNetherlands

* Corresponding Author: Kouris A I.,

European Cytokine Network 2014, 25(4), 63-68. https://doi.org/10.1684/ecn.2014.0358

Abstract

Background: Psoriasis is one of the most common, immune-mediated, chronic inflammatory skin diseases. Proinflammatory cytokines play an important pathogenetic role at a local level. Objective: To assess whether the proinflammatory cytokines IL-1β, IL-6, IL-17, IL-22 and TNF-α are released systemically during psoriasis. Methods: Peripheral blood mononuclear cells (PBMCs) were isolated from 30 patients with psoriasis and 30 healthy volunteers. Cytokine production was assessed in supernatants using an enzyme immunoassay after stimulation of PBMCs with microbial stimuli. In addition, flow cytometry was used to determine the subsets of monocytes involved and the intracellular TNF-α production in monocytes. Results: IL-17 levels were significantly higher in the supernatants of PBMCs from psoriatic patients after stimulation with phytohemagglutinin. TNF-α production was also significantly higher in cells from psoriatic patients after stimulation with all stimuli, as compared with health volunteers. Similar changes were not found for the other cytokines. A statistically significant difference was observed between patients and controls for inflammatory CD14⁺/CD16⁺ monocytes (p<0.0001) and patrolling CD14^-/CD16⁺ monocytes. Conclusion: Hyper-production of TNF-α is documented in psoriasis. These results support the concept that there is a systemic, proinflammatory component in psoriasis.

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