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Review
. 2022 Aug 26:13:961107.
doi: 10.3389/fimmu.2022.961107. eCollection 2022.

Current knowledge of the implication of lipid mediators in psoriasis

Mélissa Simard  1   2 , Sophie Morin  1   2 , Zainab Ridha  1 , Roxane Pouliot  1   2
Affiliations
Review

Current knowledge of the implication of lipid mediators in psoriasis

Mélissa Simard et al. Front Immunol. .

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.

Keywords: inflammation; lipid mediator; polyunsaturated fatty acids; psoriasis; skin.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
Skin structure and lipid metabolism. In the epidermis: 1) Fatty acids are hydrolyzed from phospholipids and transported in the endoplasmic reticulum. 2) Synthesis of more complex lipids. 3) Storage of lipids in lamellar bodies. 4) Extrusion of lamellar bodies and organization of the lipid matrix.
Figure 2
Figure 2
Schematic representation of different types of lipid mediators. Lipid mediators derived from ALA, EPA, DHA, LA, DGLA and AA. AA, arachidonic acid; ALA, alpha-linolenic acid; CYP, P450 cytochrome; DGLA, dihomo-gamma-linolenic acid; DHA, docosahexaenoic acid; DPA, docosapentaenoic acid; DTA, docosatetraenoic acid; EPA, eicosapentaenoic acid; EpDPE, epoxy-docosapentaenoic acid; EpEDE, epoxy-eicosadienoic acid; EpETE, epoxy-ecosatetraenoic acid; EpETrE, epoxy-eicosatrienoic acid; EpODE, epoxy-octadecadienoic acid; EpOME, epoxy-octadecenoic acid; ETA, eicosatetraenoic acid; GLA, gamma-linolenic acid; HDoHE, hydroxy-docosahexaenoic acid; HDHA, hydroxy-docosahexaenoic acid; HEPE, hydroxy-eicosapentaenoic acid; HETE, hydroxy-eicosatetraenoic acid; HETrE, hydroxy-eicosatrienoic acid; HODE, hydroxy-octadecadienoic acid; HOTrE, hydroxy-octadecatrienoic acid; LA, linoleic acid; SDA, stearidonic acid; TriHOME, trihydroxy-octadecenoic acid, PG, prostaglandin; LT, leukotriene; TX, thromboxane.
Figure 3
Figure 3
Hydroxy-fatty acids, leukotrienes and other lipid mediators’ biosynthetic pathways derived from EPA and AA. AA, arachidonic acid; CYP, P450 cytochrome; DiHETE, dihydroxyeicosatetraenoic acid; DiHEPE, dihydroxyeicosapentaenoic acid; EPA, eicosapentaenoic acid; Ex, eoxin; HEPE, hydroxy-eicosapentaenoic acid; HETE, hydroxy-eicosatetraenoic acid; HpETE, hydroxy-peroxy-eicoisatetraenoic acid; HpEPE, hydroxy-peroxy-eicoisapentaenoic acid; LT, leukotriene; LOX, lipoxygenase; Lx, lipoxin; oxo-ETE, oxo-eicosatetraenoic; oxo-HEPE, oxo-eicosapentaenoic.
Figure 4
Figure 4
Hydroxy fatty acids, and other lipid mediators’ biosynthetic pathways derived from DHA. DHA, docosahexaenoic acid; HDHA, hydroxy-docosahexaenoic acid; HpDHA, hydroxy-peroxy-docosahexaenoic acid; MaR, maresin; oxo-DHA, oxo-octadecatrienoic; PD, protectin; Rv, resolvin.
Figure 5
Figure 5
Establishment of the psoriatic plaque. Following a physical trauma or triggered by genetic predispositions, keratinocytes secrete their own DNA. The pDC become activated and stimulate the dermal DC. Dermal DC present their antigen to T cells, which induces T cell recruitment, CD4+ T cell polarization toward a Th1 and Th17 phenotype and CD8+ T cell migration to the epidermis. Keratinocytes enter into hyperproliferation. Neutrophils are recruited and migrate to the stratum corneum. LTB4 contributes to neutrophil chemotaxis while PGE2 contributes to keratinocyte proliferation.
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