Abstract
Endothelial progenitor cells (EPCs) repair damaged vascular endothelium, and low circulating EPC levels have been associated with cardiovascular disease (CVD). CD34(+)/KDR(+) EPCs are commonly reported in the literature and CD34(+)/CD133(+)/KDR(+) EPCs are rare in circulation but highly specific for endothelial lineage. HIV-infected (HIV+) adults have chronic inflammation and increased CVD risk, but the relationship between CVD, vascular inflammation, and EPCs in HIV remains unclear. In a pilot study, EPCs were measured in 57 HIV+ men [≥50 years old, HIV-1 RNA <50 copies/ml on antiretroviral therapy (ART)] by real-time flow cytometry using cellular immaturity (CD34 and/or CD133) and endothelial commitment (KDR) markers. Fasting inflammatory biomarker levels were measured by ELISA. Median age was 57 years; CD4(+) T lymphocyte count was 570 cells/mm(3). Prevalent CVD risk factors included 16% diabetes, 28% hypertension, 53% dyslipidemia, and 33% smoking. Median (interquartile range) EPC values were CD34(+)/KDR(+) 0.1 (0.0-0.9) cells/10(5) peripheral blood mononuclear cells (PBMCs) and CD34(+)/CD133(+)/KDR(+) 0.1 (0.0-0.9) cells/10(5) PBMCs. We observed a high prevalence of undetectable CD34(+)/KDR(+) (40%) and CD34(+)/CD133(+)/KDR(+) EPCs (44%). Men with undetectable EPCs were more likely to have ≥2 CVD risk factors, lower interleukin-6 (IL-6), and higher sCD163 levels. In these older HIV+ men on suppressive ART, CD34(+)/KDR(+) and CD34(+)/CD133(+)/KDR(+) EPC levels were low and often undetectable. Undetectable EPC levels were associated with greater CVD risk factor burden, lower IL-6 (consistent with decreased EPC production stimulus), and higher sCD163 (consistent with monocyte activation and prior CVD associations) levels, suggesting a potential relationship between EPCs and atherosclerotic burden in this population.