Abstract
The aim of this study was to investigate possible stress-associated disturbances in lipid metabolism in mononuclear cells, mainly lymphocytes of patients with psoriasis vulgaris (Ps, n = 32) or with psoriatic arthritis (PsA, n = 16) in respect to the healthy volunteers (n = 16). The results showed disturbances in lipid metabolism of psoriatic patients reflected by different phospholipid profiles. The levels of non-enzymatic lipid metabolites associated with oxidative stress 8-isoprostaglandin F2α (8-isoPGF2α) and free 4-hydroxynonenal (4-HNE) were higher in PsA, although levels of 4-HNE-His adducts were higher in Ps. In the case of the enzymatic metabolism of lipids, enhanced levels of endocannabinoids were observed in both forms of psoriasis, while higher expression of their receptors and activities of phospholipases were detected only in Ps. Moreover, cyclooxygenase-1 (COX-1) activity was enhanced only in Ps, but cyclooxygenase-2 (COX-2) was enhanced both in Ps and PsA, generating higher levels of eicosanoids: prostaglandin E1 (PGE1), leukotriene B4 (LTB4), 13-hydroxyoctadecadienoic acid (13HODE), thromboxane B2 (TXB2). Surprisingly, some of major eicosanoids 15-d-PGJ2 (15-deoxy-Δ12,14-prostaglandin J2), 15-hydroxyeicosatetraenoic acid (15-HETE) were elevated in Ps and reduced in PsA. The results of our study revealed changes in lipid metabolism with enhancement of immune system-modulating mediators in psoriatic mononuclear cells. Evaluating further differential stress responses in Ps and PsA affecting lipid metabolism and immunity might be useful to improve the prevention and therapeutic treatments of psoriasis.
Highlights
Psoriasis is a chronic autoimmune disease, the most common form of which is psoriasis vulgaris, characterized by pathological interactions between immune cells, especially lymphocytes, and skin cells, especially keratinocytes
The results of our study confirm the onset of Psoriasis is a complex inflammatory disease associated with increased activation of lymphocytes [14], which leads to the generation of pro-inflammatory cytokines and to pro-oxidative processes causing oxidative stress [3]
The results of our research suggest that the development of both forms of psoriasis is strongly associated with oxidative stress resulting in altered lipid metabolism and cytokine production, leading to the development of pro-inflammatory preconditioning of the immune cells
Summary
Psoriasis is a chronic autoimmune disease, the most common form of which is psoriasis vulgaris, characterized by pathological interactions between immune cells, especially lymphocytes, and skin cells, especially keratinocytes. It has been observed that lymphocytes and the cytokines they produce, especially interferon γ (IFNγ) and interleukin 17 (IL-17), affect other cells, leading to chronic inflammation and characteristic symptoms such as cutaneous plaques in psoriasis or arthrosis and loss of movement in psoriatic arthritis. Recent studies on immunological diseases have revealed that their development is often accompanied by oxidative stress and increased metabolism of phospholipids, suggesting that both ROS and lipid mediators play important roles in the pathophysiology of psoriasis [3]. In psoriasis, both systemic and local, oxidative stress and increased metabolism of phospholipids have been demonstrated. Biological activities of ROS are related to their ability to react with biomolecules, such as phospholipids, in particular polyunsaturated fatty acids (PUFA), which leads to lipid peroxidation and generation of reactive aldehydes, e.g., 4-hydroxynonenal (4-HNE), which is denoted as a “second messenger of free radicals” [6]
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