NDLI: Reduced CD14 expression on classical monocytes and vascular endothelial adhesion markers independently associate with carotid artery intima media thickness in chronically HIV-1 infected adults on virologically suppressive anti-retroviral therapy

Content Provider	PubMed Central
Author	Barbour, Jason D. Jalbert, Emilie C. Chow, Dominic C. Gangcuangco, Louie Mar A. Norris, Philip J. Keating, Sheila M. Heitman, John Nagamine, Lorna Seto, Todd Ndhlovu, Lishomwa C. Nakamoto, Beau K. Hodis, Howard N. Parikh, Nisha I. Shikuma, Cecilia M.
Copyright Year	2013
Abstract	HIV infection causes systemic immune inflammation, and increases the risk for cardiovascular (CVD) disease even among those on virologically suppressive anti-retroviral treatment (ART). We performed a biostatistical analysis and screen of candidate cellular and plasma biomarkers for association with carotid artery intima-media thickness (CIMT), independent of traditional CVD risk factors such as age, gender, systolic blood pressure (SBP), lipid levels, smoking and diabetes. We conducted a multi-stage analysis based on a cross-sectional study of CVD risk in HIV-infected subjects age >45 years on ART for >6 months. The goal of this analysis was to identify candidate cellular and plasma biomarkers of CIMT in HIV-1 infected adults. We further sought to determine if these candidate biomarkers were independent of traditional CVD risk factors previously identified in HIV negative adults. High-resolution B-mode ultrasound images of the right common carotid common artery (CCA) were obtained. Plasma soluble inflammatory mediators, cytokines and chemokines were detected. Monocytes were defined by CD14/CD16 expression, and CD8+ T-cell activation by CD38/HLA-DR expression. Subjects were a median of 49.5 years old, 87% male, had a CIMT of 0.73 mm, FRS of 6%, a median viral load of 48 copies/mL, and CD4+ T cell count of 479 cells/μL. Soluble VCAM-1, and expansion of CD14dimCD16− monocytes each associated with higher CIMT independently of age and SBP. These factors are distinct components of a shared atherogenic process; 1) vascular endothelial molecular expression and 2) vascular monocytes that enter into the vascular endothelium and promote atherosclerotic plaque.
Related Links	http://dx.doi.org/10.1016/j.atherosclerosis.2013.10.021
Ending Page	58
Page Count	7
Starting Page	52
File Format	PDF
ISSN	00219150
e-ISSN	18791484
Journal	Atherosclerosis
Issue Number	1
Volume Number	232
Language	English
Publisher Date	2014-01-01
Access Restriction	Open
Subject Keyword	Cardiology and Cardiovascular Medicine Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Cardiology and Cardiovascular Medicine

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