Plasma levels of adipokines in systemic lupus erythematosus patients

Highlights

• Plasma levels of the six adpokines do not differ between SLE and normal controls.

• Omentin-1 level is lower in SLE patients without nephritis.

• Chemerin and cathepsin-S level are higher in SLE with nervous system disorder.

Abstract

Objective

To evaluate the plasma levels of six adipokines, including chemerin, omentin-1, lipocalin-2, cathepsin-S, cathepsin-L and adipsin, in patients with SLE.

Methods

Ninety SLE patients and ninety control subjects were recruited, plasma adipokines levels were measured by enzyme-linked immunosorbent assay, and their associations with major clinical and laboratory indexes were analyzed.

Results

There were no significant differences in plasma chemerin, omentin-1, lipocalin-2, cathepsin-S, cathepsin-L and adipsin levels between SLE patients and controls. Further subgroup analyses by major clinical and laboratory indexes showed that plasma omentin-1 level was significantly lower in SLE patients without nephritis when compared with those patients with nephritis (P = 0.002). Plasma chemerin, cathepsin-S levels in SLE patients without nervous system disorder were significantly lower in comparison with SLE patients with nervous system disorder (P = 0.035, P = 0.029). No significant associations of other adipokines with any major clinical and laboratory indexes were observed.

Conclusions

Plasma levels of chemerin, omentin-1, lipocalin-2, cathepsin-S, cathepsin-L and adipsin in SLE patients were not markedly different from the normal controls. The presence of nephritis was connected with higher plasma omentin-1 levels in SLE patients, and the presence of nervous system disorder was associated with higher plasma chemerin, cathepsin-S levels in SLE patients. However, functional studies are awaited to further explore the potential roles of these cytokines in SLE.

Introduction

Systemic lupus erythematosus (SLE) is a chronic, recurrent, potentially fatal inflammatory connective tissue disorder characterized by the loss of self-immune tolerance, autoantibody production, formation of immune complexes, tissue inflammation in multiple organs, with high levels of pro-inflammatory cytokines in blood [1]. SLE patients have increased risk for cardiovascular events, metabolic syndrome caused by insulin resistance, and are associated with the development of obesity [2], [3], [4]. Adipose tissue has already been identified as a storage depot for body energy, but it is now also recognized as a key, complex endocrine organ by secreting a large number of mediators, including leptin, chemerin, resistin, omentin-1, etc., known as adipokines that have pro-inflammatory or anti-inflammatory effect [5]. These adipokines could affect metabolism, inflammation, and are responsible for pathological changes associated with obesity, metabolic syndrome, cardiovascular disease [6], as well as play significant roles in inflammatory, autoimmune and rheumatic diseases [5], [7].

Numerous studies have focused on the expression and pathogenic roles of several adipokines in autoimmune diseases like SLE [8], [9], [10], [11], [12]. For instance, leptin has been suggested to have a role in pathogenic process of SLE, in particular modulating the cardiovascular risk of SLE patients. One study suggested that the leptin receptor gene Q223R polymorphism and increased serum leptin levels were significantly associated with increased SLE risk [8]. Meanwhile, two contradictory findings that serum leptin levels were significantly lower in SLE patients compared to the controls, and there was no significant difference in plasma leptin levels between SLE patients and controls were also reported [9], [10]. Our recent study by meta-analysis also shows no significant difference in plasma/serum leptin levels between the SLE patients and controls [13]. Another study has demonstrated plasma adiponectin levels were increased in SLE patients with lupus nephritis (LN) in comparison with normal controls and SLE patients without LN [10], [11]. Another adipokine, resistin has also been involved in SLE but with contradictory results [14]. In addition to leptin, adiponectin and resistin, there are also other adipokines, such as chemerin, omentin-1, lipocalin-2, etc., but very little is known about the expression level and pathogenic role of these adipocytokines in SLE. Therefore, in the present study, we evaluated the plasma chemerin, omentin-1, lipocalin-2, cathepsin-S, cathepsin-L and adipsin levels and their clinical associations in patients with SLE.