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J Infect Dis. 2017 May 1;215(9):1352-1361. doi: 10.1093/infdis/jix082.

Association of Macrophage Inflammation Biomarkers With Progression of Subclinical Carotid Artery Atherosclerosis in HIV-Infected Women and Men.

Author information

1
Department of Epidemiology and Population Health, Albert Einstein College of Medicine, Bronx, New York.
2
Department of Medicine, Johns Hopkins University, Baltimore, Maryland.
3
Department of Medicine, University of Southern California, Los Angeles.
4
Department of Medicine, John H. Stroger, Jr Hospital of Cook County, Chicago, Illinois.
5
Department of Epidemiology, Johns Hopkins University, Baltimore, Maryland.
6
Department of Medicine, University of Alabama at Birmingham.
7
Department of Medicine, SUNY-Downstate Medical Center, Brooklyn, New York.
8
Department of Medicine, Georgetown University Medical Center, Washington, DC.
9
Department of Preventive Medicine, University of Southern California, Los Angeles.
10
Department of Medicine, Emory University and Grady Healthcare System, Atlanta, Georgia.
11
Department of Medicine, Northwestern University Medical Center, Chicago, Illinois.
12
Department of Medicine, University of California-San Francisco and the Department of Veterans Affairs.
13
Department of Medicine, Los Angeles Biomedical Research Institute at Harbor-UCLA, Torrance, California.
14
Department of Immunology and Microbiology, Rush University Medical Center, Chicago, Illinois.
15
Departments of Epidemiology and Infectious Diseases and Microbiology, University of Pittsburgh, Pennsylvania; and.
16
Department of Pathology and Laboratory Medicine, University of Vermont, Colchester.

Abstract

Background:

Monocytes and monocyte-derived macrophages promote atherosclerosis through increased inflammation and vascular remodeling. This may be especially true in chronic human immunodeficiency virus (HIV) infection.

Methods:

We examined 778 women (74% HIV+) in the Women's Interagency HIV Study and 503 men (65% HIV+) in the Multicenter AIDS Cohort Study who underwent repeated B-mode carotid artery ultrasound imaging in 2004-2013. We assessed baseline associations of the serum macrophage inflammation markers soluble (s)CD163, sCD14, galectin-3 (Gal-3), and Gal-3 binding protein (Gal-3BP) with carotid plaque formation (focal intima-media thickness >1.5 mm) over 7 years.

Results:

Marker levels were higher in HIV+ persons versus HIV- persons. Presence of focal plaque increased over time: from 8% to 15% in women, and 24% to 34% in men. After adjustment for demographic, behavioral, and cardiometabolic factors, and CRP and interleukin-6, each standard deviation increase in sCD14 was associated with increased plaque formation (risk ratio [RR] 1.24, 95% confidence interval [CI] 1.07-1.43). This pattern was consistentby sex. sCD163 was associated with plaque formation in virally suppressed HIV+ men (RR 1.52, 95% CI 1.04-2.22); Gal-3BP and Gal-3 were not associated with increased plaque.

Conclusions:

sCD14 and sCD163 may play important roles in atherogenesis among HIV+ persons.

KEYWORDS:

HIV infection; atherosclerosis; galectin-3; galectin-3 binding protein; inflammation; intima-media thickness; macrophages; monocytes; soluble CD14; soluble CD163.

PMID:
28199691
PMCID:
PMC5722037
DOI:
10.1093/infdis/jix082
[Indexed for MEDLINE]
Free PMC Article

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