Abstract
BackgroundIn this study, the effect of 15-month anti-tumor necrosis factor alpha (TNF-α) treatment on circulating levels of plasma sulfated glycosaminoglycans (GAGs) and the nonsulfated GAG hyaluronic acid (HA) in female rheumatoid arthritis (RA) patients was assessed.MethodsPlasma was obtained from healthy subjects and RA women treated with TNF-α antagonists (etanercept or adalimumab or certolizumab pegol) in combination with methotrexate. GAGs were isolated from plasma samples using ion exchange low-pressure liquid chromatography. Total sulfated GAGs were quantified using a hexuronic acid assay. Plasma levels of keratan sulfate (KS) and HA were measured using immunoassay kits.ResultsTotal sulfated GAGs and HA levels were higher in female RA patients before treatment in comparison to healthy subjects. KS levels did not differ between RA women and controls. Anti-TNF-α treatment resulted in normalization of plasma total GAG and HA levels in RA patients, without any effect on KS levels.ConclusionsOur results suggest that anti-TNF-α therapy has a beneficial effect on extracellular matrix remodeling in the course of RA.
Highlights
In this study, the effect of 15-month anti-tumor necrosis factor alpha (TNF-α) treatment on circulating levels of plasma sulfated glycosaminoglycans (GAGs) and the nonsulfated GAG hyaluronic acid (HA) in female rheumatoid arthritis (RA) patients was assessed
Clinical response Out of a total of 45 female RA patients recruited for the study, 16 patients were excluded and the remaining 29 patients completed 15 months of treatment with TNF-α inhibitors (TNFαI)
29 female RA patients who continued the TNFαI therapy for 15 months were included in our analysis and are presented in this study
Summary
The effect of 15-month anti-tumor necrosis factor alpha (TNF-α) treatment on circulating levels of plasma sulfated glycosaminoglycans (GAGs) and the nonsulfated GAG hyaluronic acid (HA) in female rheumatoid arthritis (RA) patients was assessed. Some of the integral elements of chronic inflammation are the structural and functional changes in extracellular matrix (ECM) compounds, including proteoglycans (PGs) and their sugar constituents—that is, glycosaminoglycans (GAGs) [8, 9] The latter are negatively charged unbranched polysaccharides consisting of repeating disaccharide units of hexosamine and uronic acid or galactose. All GAG types, except HA, are Szeremeta et al Arthritis Research & Therapy (2018) 20:211 covalently attached to the core protein, forming PGs, and exhibit various degrees of sulfation along the polysaccharide chain [10,11,12] This structural heterogeneity allows GAGs to interact with and modify the actions of numerous cell-adhesion molecules, growth factors, cytokines, chemokines, components of ECM, proteases, and their inhibitors, which underlie their important biological functions, including cellular communication, cell signaling, and regulation of other biochemical pathways [10, 13]. Jura-Półtorak et al [15] described an increase in the total plasma GAG level in patients with RA
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