Current knowledge of the implication of lipid mediators in psoriasis

Abstract

The skin is an organ involved in several biological processes essential to the proper functioning of the organism. One of these essential biological functions of the skin is its barrier function, mediated notably by the lipids of the stratum corneum, and which prevents both penetration from external aggression, and transepidermal water loss. Bioactive lipid mediators derived from polyunsaturated fatty acids (PUFAs) constitute a complex bioactive lipid network greatly involved in skin homeostasis. Bioactive lipid mediators derived from n-3 and n-6 PUFAs have well-documented anti- and pro-inflammatory properties and are recognized as playing numerous and complex roles in the behavior of diverse skin diseases, including psoriasis. Psoriasis is an inflammatory autoimmune disease with many comorbidities and is associated with enhanced levels of pro-inflammatory lipid mediators. Studies have shown that a high intake of n-3 PUFAs can influence the development and progression of psoriasis, mainly by reducing the severity and frequency of psoriatic plaques. Herein, we provide an overview of the differential effects of n-3 and n-6 PUFA lipid mediators, including prostanoids, hydroxy-fatty acids, leukotrienes, specialized pro-resolving mediators, N-acylethanolamines, monoacylglycerols and endocannabinoids. This review summarizes current findings on lipid mediators playing a role in the skin and their potential as therapeutic targets for psoriatic patients.

Abnormalities of Sphingolipids Metabolic Pathways in the Pathogenesis of Psoriasis

“…In the present study, we present a resume of the main finds of these genes related to psoriasis. For more detailed information about fatty acid metabolism and psoriasis, we suggest considering Sorokin et al, 2018; Rioux et al, 2020; and Simard et al, 2022 [ 79 , 80 , 81 ].…”

Current developments and perspectives in psoriasis

“…The innate immune system is represented, for example, by macrophages, neutrophilic granulocytes, and (plasmacytoid) dendritic cells, and the adaptive immune system by T lymphocytes, especially Th17 cells. Communication between these immune cells is mediated by various cytokines, chemokines, and other mediators 31 . Among these, tumor necrosis factor alpha (TNF‐α) and components of the interleukin (IL)‐23/IL‐17 axis, in particular, have been established as major pathogenesis‐oriented therapeutic targets for several years (Figure 1).…”

“…Communication between these immune cells is mediated by various cytokines, chemokines, and other mediators. 31 Among these, tumor necrosis factor alpha (TNF-α) and components of the interleukin (IL)-23/IL-17 axis, in particular, have been established as major pathogenesis-oriented therapeutic targets for several years (Figure 1). [32][33][34][35] Approved biologics are etanercept, infliximab, adalimumab, certolizumab pegol, and golimumab (the latter F I G U R E 1 Schematic and simplified representation of the mechanisms of action of current antipsoriatic drugs.…”

Aktuelle Entwicklungen und Perspektiven bei Psoriasis

“…29,30 Der angeborene Schenkel des Immunsystems wird beispielsweise durch Makrophagen, neutrophile Granulozyten und (plasmazytoide) dendritische Zellen repräsentiert, der adaptive durch T-Lymphozyten, vor allem Th17-Zellen. Die Kommunikation zwischen diesen Immunzellen wird durch verschiedene Zytokine, Chemokine und andere Mediatoren, 31 vermittelt, wobei insbesondere Tumor-Nekrose-Faktor (TNF)-α und Komponenten der Interleukin (IL)-23/IL-17-Achse seit einigen Jahren als wesentliche pathogeneseorientierte therapeutische Zielstrukturen etabliert sind (Abbildung 1). [32][33][34][35] Derzeit zugelassene Biologika sind Etanercept, Infliximab, Adalimumab, Certolizumab Pegol sowie Golimumab (letzteres nur für Psoriasis-Arthritis [PsA]) gegen TNF-α, Secukinumab und Ixekizumab gegen IL-17A, Bimekizumab gegen IL-17A und IL-17F, Brodalumab gegen den IL-17-Rezeptor a/c, Ustekinumab gegen IL-12 und IL-23 sowie Guselkumab, Tildrakizumab und Risankizumab gegen IL-23.…”