Abstract
Psoriasis and obesity, while distinct, are inter-related inflammatory conditions. Adipose tissue (AT)-derived mediators could be pathogenically active in triggering and/or amplifying psoriatic skin inflammation and, vice versa, skin inflammation could drive increased adiposity that triggers the development of several chronic conditions. Gaining insight into their intricate relationship could be essential for effective management and treatment. The aim of this study was to determine (i) the pathogenic role of psoriasis-signature cytokines in contributing to AT metabolism and (ii) the role of AT-derived mediators in triggering and/or amplifying skin inflammation. For this reason, firstly, whole AT was treated with IL-17 and TNF-α, alone or in combination, to investigate their effects on the expression and production of adipokines and inflammatory factors. IL-17 and TNF-α were able to induce an additive or synergistic effect on AT-derived mediators. In order to assess the effects on the skin of inflamed AT by psoriasis-signature cytokines, ex vivo skin organ culture was performed and an increase in several inflammatory mediators was observed. These findings confirm that psoriasis and obesity amplify each other's inflammatory processes and understanding this mutual exacerbation could lead to more effective therapeutic strategies that address both skin inflammation and AT metabolism.