Affiliation:
1. School of Health and Rehabilitation Sciences, Division of Medical Laboratory Science, Ohio State University, Columbus
2. National Health Laboratory Service and Faculty of Health Sciences, University of Witwatersrand, Johannesburg
3. Harrington Heart & Vascular Institute, University Hospitals Case Medical Center, Cleveland, Ohio
4. Department of Medicine, Division of Infectious Diseases, Ohio State University, Columbus
5. Department of Internal Medicine, Division of Infectious Diseases, Case Western Reserve University/University Hospitals of Cleveland, Ohio
Abstract
Abstract
Background
Human immunodeficiency virus (HIV)-infected individuals have increased risk for vascular thrombosis, potentially driven by interactions between activated leukocytes and the endothelium.
Methods
Monocyte subsets (CD14+CD16−, CD14+CD16+, CD14DimCD16+) from HIV negative (HIV−) and antiretroviral therapy-treated HIV positive (HIV+) participants (N = 19 and 49) were analyzed by flow cytometry for adhesion molecule expression (lymphocyte function-associated antigen 1 [LFA-1], macrophage-1 antigen [Mac-1], CD11c/CD18, very late antigen [VLA]-4) and the fractalkine receptor (CX3CR1); these receptors recognize ligands (intercellular adhesion molecules [ICAMs], vascular cell adhesion molecule [VCAM]-1, fractalkine) on activated endothelial cells (ECs) and promote vascular migration. Plasma markers of monocyte (soluble [s]CD14, sCD163) and EC (VCAM-1, ICAM-1,2, fractalkine) activation and systemic (tumor necrosis factor receptor [TNFR-I], TNFR-II) and vascular (lipoprotein-associated phospholipase A2 [Lp-PLA2]) inflammation were measured by enzyme-linked immunosorbent assay.
Results
Proportions of CD16+ monocyte subsets were increased in HIV+ participants. Among all monocyte subsets, levels of LFA-1 were increased and CX3CR1 levels were decreased in HIV+ participants (P < .01). Levels of sCD163, sCD14, fractalkine, ICAM-1, VCAM-1, TNFR-II, and Lp-PLA2 were also increased in HIV+ participants (P < .05), and levels of sCD14, TNFR-I, and TNFR-II were directly related to ICAM-1 and VCAM-1 levels in HIV+ participants. Expression of CX3CR1 on monocyte subsets was inversely related to plasma Lp-PLA2 (P < .05 for all).
Conclusions
Increased proportions of CD16+ monocytes, cells with altered adhesion molecule expression, combined with elevated levels of their ligands, may promote vascular inflammation in HIV infection.
Funder
National Institutes of Health
AIDS Clinical Trials Group’s Minority Investigator
Fasenmyer Foundation
Center for AIDS Research
Clinical and Translational Science Collaborative
National Center for Advancing Translational Sciences
Publisher
Oxford University Press (OUP)
Subject
Infectious Diseases,Oncology
Cited by
33 articles.
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