T P Mikołajczyk1, G Osmenda1, B Batko2, G Wilk1, M Krezelok2, D Skiba3, T Sliwa1, J R Pryjma4, T J Guzik5. 1. Translational Medicine Laboratory, Department of Internal Medicine, Jagiellonian University School of Medicine, Krakow, Poland. 2. Division of Rheumatology, J Dietl Clinical Hospital, Krakow, Poland. 3. Translational Medicine Laboratory, Department of Internal Medicine, Jagiellonian University School of Medicine, Krakow, Poland Institute of Cardiovascular and Medical Sciences, University of Glasgow, UK. 4. Department of Immunology, Faculty of Biochemistry, Biophysics and Biotechnology, Jagiellonian University, Krakow, Poland. 5. Translational Medicine Laboratory, Department of Internal Medicine, Jagiellonian University School of Medicine, Krakow, Poland Institute of Cardiovascular and Medical Sciences, University of Glasgow, UK t.guzik@uj.edu.pl.
Abstract
BACKGROUND: Systemic lupus erythematosus (SLE) is characterized by increased cardiovascular morbidity and mortality. SLE patients have increased prevalence of subclinical atherosclerosis, although the mechanisms of this observation remain unclear. Considering the emerging role of monocytes in atherosclerosis, we aimed to investigate the relationship between subclinical atherosclerosis, endothelial dysfunction and the phenotype of peripheral blood monocytes in SLE patients. METHODS: We characterized the phenotype of monocyte subsets defined by the expression of CD14 and CD16 in 42 patients with SLE and 42 non-SLE controls. Using ultrasonography, intima-media thickness (IMT) of carotid arteries and brachial artery flow-mediated dilation (FMD) as well as nitroglycerin-induced dilation (NMD) were assessed. RESULTS: Patients with SLE had significantly, but only modestly, increased IMT when compared with non-SLE controls (median (25th/75th percentile) 0.65 (0.60/0.71) mm vs 0.60 (0.56/0.68) mm; p < 0.05). Importantly, in spite of early atherosclerotic complications in the studied SLE group, marked endothelial dysfunction was observed. CD14dimCD16+proinflammatory cell subpopulation was positively correlated with IMT in SLE patients. This phenomenon was not observed in control individuals. Interestingly, endothelial dysfunction assessed by FMD was not correlated with any of the studied monocyte subsets. CONCLUSIONS: Our observations suggest that CD14dimCD16+monocytes are associated with subclinical atherosclerosis in SLE, although the mechanism appears to be independent of endothelial dysfunction.
BACKGROUND:Systemic lupus erythematosus (SLE) is characterized by increased cardiovascular morbidity and mortality. SLEpatients have increased prevalence of subclinical atherosclerosis, although the mechanisms of this observation remain unclear. Considering the emerging role of monocytes in atherosclerosis, we aimed to investigate the relationship between subclinical atherosclerosis, endothelial dysfunction and the phenotype of peripheral blood monocytes in SLEpatients. METHODS: We characterized the phenotype of monocyte subsets defined by the expression of CD14 and CD16 in 42 patients with SLE and 42 non-SLE controls. Using ultrasonography, intima-media thickness (IMT) of carotid arteries and brachial artery flow-mediated dilation (FMD) as well as nitroglycerin-induced dilation (NMD) were assessed. RESULTS:Patients with SLE had significantly, but only modestly, increased IMT when compared with non-SLE controls (median (25th/75th percentile) 0.65 (0.60/0.71) mm vs 0.60 (0.56/0.68) mm; p < 0.05). Importantly, in spite of early atherosclerotic complications in the studied SLE group, marked endothelial dysfunction was observed. CD14dimCD16+proinflammatory cell subpopulation was positively correlated with IMT in SLEpatients. This phenomenon was not observed in control individuals. Interestingly, endothelial dysfunction assessed by FMD was not correlated with any of the studied monocyte subsets. CONCLUSIONS: Our observations suggest that CD14dimCD16+monocytes are associated with subclinical atherosclerosis in SLE, although the mechanism appears to be independent of endothelial dysfunction.
Authors: Grzegorz Wilk; Grzegorz Osmenda; Paweł Matusik; Daniel Nowakowski; Barbara Jasiewicz-Honkisz; Adam Ignacak; Marta Cześnikiewicz-Guzik; Tomasz J Guzik Journal: Pol Arch Med Wewn Date: 2013-09-11
Authors: Kyrill S Rogacev; Christof Ulrich; Lutz Blömer; Florian Hornof; Katrin Oster; Maren Ziegelin; Bodo Cremers; Yvonne Grenner; Jürgen Geisel; Axel Schlitt; Hans Köhler; Danilo Fliser; Matthias Girndt; Gunnar H Heine Journal: Eur Heart J Date: 2009-08-17 Impact factor: 29.983
Authors: Fabian C Franzeck; Danielle Hof; Remo D Spescha; Matthias Hasun; Alexander Akhmedov; Jan Steffel; Yi Shi; Francesco Cosentino; Felix C Tanner; Arnold von Eckardstein; Willibald Maier; Thomas F Lüscher; Christophe A Wyss; Giovanni G Camici Journal: Atherosclerosis Date: 2011-11-02 Impact factor: 5.162
Authors: Kyrill S Rogacev; Sarah Seiler; Adam M Zawada; Birgit Reichart; Esther Herath; Daniel Roth; Christof Ulrich; Danilo Fliser; Gunnar H Heine Journal: Eur Heart J Date: 2010-10-12 Impact factor: 29.983
Authors: Stefan Frantz; Ulrich Hofmann; Daniela Fraccarollo; Andreas Schäfer; Stefanie Kranepuhl; Ina Hagedorn; Bernhard Nieswandt; Matthias Nahrendorf; Helga Wagner; Barbara Bayer; Christina Pachel; Michael P Schön; Susanne Kneitz; Tobias Bobinger; Frank Weidemann; Georg Ertl; Johann Bauersachs Journal: FASEB J Date: 2012-11-16 Impact factor: 5.191
Authors: Maureen McMahon; Brian J Skaggs; Lori Sahakian; Jennifer Grossman; John FitzGerald; Nagesh Ragavendra; Christina Charles-Schoeman; Marissa Chernishof; Alan Gorn; Joseph L Witztum; Weng Kee Wong; Michael Weisman; Daniel J Wallace; Antonio La Cava; Bevra H Hahn Journal: Ann Rheum Dis Date: 2011-06-13 Impact factor: 19.103
Authors: Pawel Maga; Tomasz P Mikolajczyk; Lukasz Partyka; Marek Krzanowski; Krzysztof P Malinowski; Rafal Nizankowski Journal: Biomed Res Int Date: 2016-10-13 Impact factor: 3.411