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      Visfatin and chemerin levels correspond with inflammation and might reflect the bridge between metabolism, inflammation and fibrosis in patients with systemic sclerosis

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          Adipokines are regulatory molecules which act as mediators of the inflammatory, fibrotic and metabolic processes by interacting with the immune system.


          We hypothesized that chemerin and visfatin by pro-inflammatory properties play a significant role in inflammation in systemic sclerosis. To address this hypothesis, we determined serum chemerin and visfatin levels in SSc patients, compared with the control group and defined the correlations with clinical and laboratory parameters in SSc patients.

          Material and methods

          The study included 48 Caucasian female patients with SSc and 38 healthy subjects of the control group. Serum concentrations of selected adipokines were measured using commercially available ELISA Kits.


          Patients with SSc had higher chemerin levels (209.38 ±55.35 ng/ml) than the control group (182.71 ±33.94 ng/ml) and the difference was statistically significant ( Z = 2.14, p = 0.032). The highest chemerin levels were found in dcSSc patients (242.46 ±95.82 ng/ml). We indicated a positive correlation of chemerin and visfatin with levels of inflammatory markers: CRP ( r = 0.35, p = 0.013 for chemerin; r = 0.41, p = 0.003 for visfatin) and ESR ( r = 0.31, p = 0.03 for chemerin; r = 0.30, p = 0.03 for visfatin). What is more, chemerin manifested a statistically significant positive correlation with the concentration of complement component C3 ( r = 0.47, p = 0.001) and C4 ( r = 0.29, p = 0.049), whereas visfatin correlated with C4 levels ( r = 0.32, p = 0.029).


          The results of our study indicate that chemerin and visfatin as pro-inflammatory cytokines might represent new markers corresponding with inflammation in systemic sclerosis and might reflect the bridge between metabolism, inflammation and potentially, chemerin may also link inflammation with skin and lung fibrosis.

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          Most cited references 74

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          Preliminary criteria for the classification of systemic sclerosis (scleroderma). Subcommittee for scleroderma criteria of the American Rheumatism Association Diagnostic and Therapeutic Criteria Committee.

          A multicenter, ongoing study of early-diagnosed cases of systemic sclerosis and comparison patients with systemic lupus erythematosus, polymyositis/dermatomyositis, and Raynaud's phenomenon was conducted in order to develop classification criteria for systemic sclerosis. Preliminary criteria are proposed namely, the finding of either the sole major criterion, i.e., proximal scleroderma, or two or more of the minor criteria, i.e., 1) sclerodactyly, 2) digital pitting scars of fingertips or loss of substance of the distal finger pad, and 3) bilateral basilar pulmonary fibrosis. When applied to the case and comparison patients included in this study, these proposed criteria had a 97% sensitivity for definite systemic sclerosis and 98% specificity.
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            Visfatin: a protein secreted by visceral fat that mimics the effects of insulin.

            Fat tissue produces a variety of secreted proteins (adipocytokines) with important roles in metabolism. We isolated a newly identified adipocytokine, visfatin, that is highly enriched in the visceral fat of both humans and mice and whose expression level in plasma increases during the development of obesity. Visfatin corresponds to a protein identified previously as pre-B cell colony-enhancing factor (PBEF), a 52-kilodalton cytokine expressed in lymphocytes. Visfatin exerted insulin-mimetic effects in cultured cells and lowered plasma glucose levels in mice. Mice heterozygous for a targeted mutation in the visfatin gene had modestly higher levels of plasma glucose relative to wild-type littermates. Surprisingly, visfatin binds to and activates the insulin receptor. Further study of visfatin's physiological role may lead to new insights into glucose homeostasis and/or new therapies for metabolic disorders such as diabetes.
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              Specific Recruitment of Antigen-presenting Cells by Chemerin, a Novel Processed Ligand from Human Inflammatory Fluids

              Dendritic cells (DCs) and macrophages are professional antigen-presenting cells (APCs) that play key roles in both innate and adaptive immunity. ChemR23 is an orphan G protein–coupled receptor related to chemokine receptors, which is expressed specifically in these cell types. Here we present the characterization of chemerin, a novel chemoattractant protein, which acts through ChemR23 and is abundant in a diverse set of human inflammatory fluids. Chemerin is secreted as a precursor of low biological activity, which upon proteolytic cleavage of its COOH-terminal domain, is converted into a potent and highly specific agonist of ChemR23, the chemerin receptor. Activation of chemerin receptor results in intracellular calcium release, inhibition of cAMP accumulation, and phosphorylation of p42–p44 MAP kinases, through the Gi class of heterotrimeric G proteins. Chemerin is structurally and evolutionary related to the cathelicidin precursors (antibacterial peptides), cystatins (cysteine protease inhibitors), and kininogens. Chemerin was shown to promote calcium mobilization and chemotaxis of immature DCs and macrophages in a ChemR23-dependent manner. Therefore, chemerin appears as a potent chemoattractant protein of a novel class, which requires proteolytic activation and is specific for APCs.

                Author and article information

                Postepy Dermatol Alergol
                Postepy Dermatol Alergol
                Advances in Dermatology and Allergology/Postȩpy Dermatologii i Alergologii
                Termedia Publishing House
                06 November 2019
                October 2019
                : 36
                : 5
                : 551-565
                [1 ]Department of Dermatology, Venereology and Pediatric Dermatology, Medical University of Lublin, Lublin, Poland
                [2 ]Department of Psychiatric Nursing, Medical University of Lublin, Lublin, Poland
                Author notes
                Address for correspondence: Karolina Sawicka MD, Department of Dermatology, Venereology and Pediatric Dermatology, Medical University of Lublin, 13 Radziwiłłowska St, 20-080 Lublin, Poland. phone/fax: +48 81 532 36 47. e-mail: k.sawicka10@ 123456gmail.com
                Copyright: © 2018 Termedia Sp. z o. o.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0) License, allowing third parties to copy and redistribute the material in any medium or format and to remix, transform, and build upon the material, provided the original work is properly cited and states its license.

                Original Paper

                visfatin, chemerin, systemic sclerosis


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