Di Caprio Roberta, Nigro Ersilia, Di Brizzi Eugenia Veronica, Buononato Dario, Mallardo Marta, Tancredi Vittorio, Daniele Aurora, Balato Anna
Unit of Dermatology, University of Campania Luigi Vanvitelli, 80138 Naples, Italy.
Department of Molecular and Biotechnological Medicine, University of Naples "Federico II", 80131 Naples, Italy.
Int J Mol Sci. 2024 Dec 15;25(24):13435. doi: 10.3390/ijms252413435.
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.
银屑病和肥胖虽然不同，但却是相互关联的炎症性疾病。脂肪组织（AT）衍生的介质可能在引发和/或放大银屑病皮肤炎症方面具有致病活性，反之，皮肤炎症可能导致肥胖增加，进而引发多种慢性疾病的发展。深入了解它们之间错综复杂的关系对于有效管理和治疗至关重要。本研究的目的是确定（i）银屑病特征性细胞因子在AT代谢中的致病作用，以及（ii）AT衍生介质在引发和/或放大皮肤炎症中的作用。因此，首先，将整个AT单独或联合用IL-17和TNF-α处理，以研究它们对脂肪因子和炎症因子表达及产生的影响。IL-17和TNF-α能够对AT衍生介质产生相加或协同作用。为了评估银屑病特征性细胞因子对炎症性AT皮肤的影响，进行了离体皮肤器官培养，并观察到几种炎症介质增加。这些发现证实银屑病和肥胖会相互放大彼此的炎症过程，理解这种相互加剧的情况可能会带来更有效的治疗策略，既能解决皮肤炎症，又能解决AT代谢问题。
