Table of Contents Author Guidelines Submit a Manuscript
Mediators of Inflammation
Volume 2013, Article ID 537539, 8 pages
http://dx.doi.org/10.1155/2013/537539
Research Article

Effect of Therapeutic Inhibition of TNF on Circulating Endothelial Progenitor Cells in Patients with Rheumatoid Arthritis

1Department of Internal Medicine and Medical Specialities, Rheumatology Unit, Sapienza Università di Roma, Viale del Policlinico 155, 00161 Roma, Italy
2Section of Biomarkers in Degenerative Diseases, Department of Cell Biology and Neurosciences, Istituto Superiore di Sanità, Viale Regina Elena 299, 00161 Rome, Italy
3Department of Cardiovascular and Respiratory Sciences, Sapienza University of Rome, Viale del Policlinico 155, 00161 Roma, Italy

Received 30 May 2013; Revised 19 July 2013; Accepted 5 August 2013

Academic Editor: Chaim Putterman

Copyright © 2013 F. R. Spinelli et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Endothelial dysfunction has been detected in RA patients and seems to be reversed by control of inflammation. Low circulating endothelial progenitor cells (EPCs) have been described in many conditions associated with increased cardiovascular risk, including RA. The aim of this study was to investigate the effect of inhibition of TNF on EPCs in RA patients. Seventeen patients with moderate-severe RA and 12 sex and age-matched controls were evaluated. Endothelial biomarkers were tested at baseline and after 3 months. EPCs were identified from peripheral blood mononuclear cells by cytofluorimetry using anti-CD34 and anti-vascular endothelial growth factor-receptor 2. Asymmetric dimethylarginine (ADMA) was tested by ELISA and flow-mediated dilatation (FMD) by ultrasonography. Circulating EPCs were significantly lower in RA patients than in controls ( ). After 3 months EPCs increased significantly ( ) while ADMA levels significantly decreased ( ). An inverse correlation between mean increase in EPCs number and mean decrease of DAS28 after treatment was observed ( , ). EPCs inversely correlated with ADMA ( , ). No improvement of FMD was detected. Short-term treatment with anti-TNF was able to increase circulating EPCs concurrently with a proportional decrease of disease activity suggesting that therapeutic intervention aimed at suppressing the inflammatory process might positively affect the endothelial function.