Premium
Markers of inflammation and CD8 T ‐cell activation, but not monocyte activation, are associated with subclinical carotid artery disease in HIV ‐infected individuals
Author(s) -
Longenecker CT,
Funderburg NT,
Jiang Y,
Debanne S,
Storer N,
Labbato DE,
Lederman MM,
McComsey GA
Publication year - 2013
Publication title -
hiv medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.53
H-Index - 79
eISSN - 1468-1293
pISSN - 1464-2662
DOI - 10.1111/hiv.12013
Subject(s) - medicine , interquartile range , fibrinogen , cd38 , cd8 , inflammation , gastroenterology , c reactive protein , endothelial activation , immunology , endocrinology , immune system , stem cell , biology , cd34 , genetics
Objectives The aim of the study was to explore the relationships between lymphocyte and monocyte activation, inflammation, and subclinical vascular disease among HIV ‐1‐infected patients on antiretroviral therapy ( ART ). Methods Baseline mean common carotid artery ( CCA ) intima‐media thickness ( IMT ) and carotid plaque ( IMT > 1.5cm) were evaluated in the first 60 subjects enrolled in the S topping A therosclerosis and T reating U nhealthy B one with R osuvastatin in HIV ( SATURN‐HIV ) trial. All subjects were adults on stable ART with evidence of heightened T ‐cell activation ( CD8 + CD38 + HLA‐DR + ≥ 19%) or increased inflammation (high‐sensitivity C ‐reactive protein ≥ 2mg/ L ). All had fasting low‐density lipoprotein ( LDL ) cholesterol ≤ 130mg/ dL . Results Seventy‐eight per cent of patients were men and 65% were A frican‐ A merican. Median (interquartile range) age and CD 4 count were 47 (43, 52) years and 648 (511, 857) cells/ μL , respectively. All had HIV ‐1 RNA < 400 HIV ‐1 RNA copies/ mL . Mean CCA‐IMT was correlated with log‐transformed CD8 + CD38 + HLA‐DR + percentage ( r = 0.326; P = 0.043), and concentrations of interleukin‐6 ( r = 0.283; P = 0.028), soluble vascular cell adhesion molecule (sVCAM; r = 0.434; P = 0.004), tumour necrosis factor‐α receptor‐ I ( TNFR ‐ I ; r = 0.591; P < 0.0001) and fibrinogen ( r = 0.257; P = 0.047). After adjustment for traditional cardiovascular disease ( CVD ) risk factors, the association with TNFR ‐ I ( P = 0.007) and fibrinogen ( P = 0.033) remained significant. Subjects with plaque ( n = 22; 37%) were older [mean (standard deviation) 51 (7.7) vs. 43 (9.4) years, respectively; P = 0.002], and had a higher CD8 + CD38 + HLA‐DR + percentage [median (interquartile range) 31% (24, 41%) vs. 23% (20, 29%), respectively; P = 0.046] and a higher sVCAM concentration [mean (standard deviation) 737 (159) vs. 592 (160) ng/ mL , respectively; P = 0.008] compared with those without plaque. Pro‐inflammatory monocyte subsets and serum markers of monocyte activation (soluble CD163 and soluble CD14 ) were not associated with CCA‐IMT or plaque. Conclusions Participants in SATURN‐HIV have a high level of inflammation and immune activation that is associated with subclinical vascular disease despite low serum LDL cholesterol.