Inflammatory biomarkers and subclinical carotid atherosclerosis in HIV-infected and HIV-uninfected men in the Multicenter AIDS Cohort Study.

Adult Aged Biomarkers / blood Carotid Artery Diseases / diagnostic imaging Cohort Studies HIV Infections / complications Humans Male Middle Aged Regression Analysis

Journal

PloS one
ISSN: 1932-6203
Titre abrégé: PLoS One
Pays: United States
ID NLM: 101285081

Informations de publication

Date de publication:
2019
Historique:
received: 24 10 2018
accepted: 19 03 2019
entrez: 5 4 2019
pubmed: 5 4 2019
medline: 21 1 2020
Statut: epublish

Résumé

HIV-infected persons have an increased risk of atherosclerosis relative to uninfected individuals. Inflammatory processes may contribute to this risk. We evaluated the associations of 10 biomarkers of systemic inflammation (CRP, IL-6, sTNF-αR1 and 2), monocyte activation (CCL2, sCD163, sCD14), coagulation (fibrinogen, D-dimer), and endothelial dysfunction (ICAM-1) with subclinical carotid atherosclerosis among participants in the Multicenter AIDS Cohort Study (MACS). Carotid plaque and intima media thickness (IMT) in the common carotid (CCA-IMT) and bifurcation region were assessed by B mode ultrasound among 452 HIV-infected and 276 HIV-uninfected men from 2010-2013. Associations between levels of each biomarker and presence of focal plaque and IMT were assessed by logistic and linear regression models, adjusting for demographics, risk behaviors, traditional cardiovascular disease (CVD) risk factors, and HIV disease characteristics. Compared to HIV-uninfected men, HIV-infected men had significantly higher levels of 8 of the 10 biomarkers. Overall, men with sCD163, CCL2, IL-6, and CRP levels in the highest quintile had approximately 2 times the odds of carotid plaque relative to those with levels in the lowest quintile, independent of demographic and CVD risk factors. Fibrinogen levels were positively associated with CCA-IMT while ICAM-1, CCL2, and sTNF-αR1 levels were positively associated with bifurcation-IMT. Among HIV-uninfected men, higher levels of sTNF-αR2 were positively associated with CCA-IMT, fibrinogen with bifurcation-IMT and carotid plaque, and ICAM-1 with carotid plaque. In addition to greater levels of systemic inflammation, heightened monocyte activation (sCD163, CCL2) may contribute to the burden of atherosclerosis among HIV-infected persons.

Sections du résumé

BACKGROUND
HIV-infected persons have an increased risk of atherosclerosis relative to uninfected individuals. Inflammatory processes may contribute to this risk. We evaluated the associations of 10 biomarkers of systemic inflammation (CRP, IL-6, sTNF-αR1 and 2), monocyte activation (CCL2, sCD163, sCD14), coagulation (fibrinogen, D-dimer), and endothelial dysfunction (ICAM-1) with subclinical carotid atherosclerosis among participants in the Multicenter AIDS Cohort Study (MACS).
METHODS
Carotid plaque and intima media thickness (IMT) in the common carotid (CCA-IMT) and bifurcation region were assessed by B mode ultrasound among 452 HIV-infected and 276 HIV-uninfected men from 2010-2013. Associations between levels of each biomarker and presence of focal plaque and IMT were assessed by logistic and linear regression models, adjusting for demographics, risk behaviors, traditional cardiovascular disease (CVD) risk factors, and HIV disease characteristics.
RESULTS
Compared to HIV-uninfected men, HIV-infected men had significantly higher levels of 8 of the 10 biomarkers. Overall, men with sCD163, CCL2, IL-6, and CRP levels in the highest quintile had approximately 2 times the odds of carotid plaque relative to those with levels in the lowest quintile, independent of demographic and CVD risk factors. Fibrinogen levels were positively associated with CCA-IMT while ICAM-1, CCL2, and sTNF-αR1 levels were positively associated with bifurcation-IMT. Among HIV-uninfected men, higher levels of sTNF-αR2 were positively associated with CCA-IMT, fibrinogen with bifurcation-IMT and carotid plaque, and ICAM-1 with carotid plaque.
CONCLUSION
In addition to greater levels of systemic inflammation, heightened monocyte activation (sCD163, CCL2) may contribute to the burden of atherosclerosis among HIV-infected persons.

Identifiants

DOI: 10.1371/journal.pone.0214735 PMID: 30946765 PMC: PMC6448851
pubmed: 30946765
doi: 10.1371/journal.pone.0214735
pii: PONE-D-18-30787
pmc: PMC6448851
doi:

Substances chimiques

Biomarkers 0

Types de publication

Journal Article Multicenter Study Research Support, N.I.H., Extramural

Langues

eng

Sous-ensembles de citation

IM

Pagination

e0214735

Subventions

Organisme : NIAID NIH HHS
ID : U01 AI035042
Pays : United States
Organisme : NIAID NIH HHS
ID : U01 AI035041
Pays : United States
Organisme : NCATS NIH HHS
ID : UL1 TR001881
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL095129
Pays : United States
Organisme : NHLBI NIH HHS
ID : U01 HL146201
Pays : United States
Organisme : NCATS NIH HHS
ID : UL1 TR001079
Pays : United States
Organisme : NIAID NIH HHS
ID : U01 AI035040
Pays : United States
Organisme : NIAID NIH HHS
ID : UM1 AI035043
Pays : United States
Organisme : NIAID NIH HHS
ID : U01 AI035039
Pays : United States

Déclaration de conflit d'intérêts

FJP is a consultant and/or on the speakers bureau for Gilead, Janssen, ViiV and Merck. This does not alter our adherence to PLOS ONE policies on sharing data and materials.

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Auteurs

Vinita Subramanya (V)

Division of Cardiology, Johns Hopkins School of Medicine, Baltimore, Maryland, United States of America.
ORCID: 0000-0002-1059-0847

Heather S McKay (HS)

Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland, United States of America.

Rebeccah M Brusca (RM)

Department of Medicine, Johns Hopkins School of Medicine, Baltimore, Maryland, United States of America.

Frank J Palella (FJ)

Division of Infectious Diseases, Northwestern University, Feinberg School of Medicine, Chicago, Illinois, United States of America.

Lawrence A Kingsley (LA)

Department of Epidemiology, University of Pittsburgh School of Public Health, Pittsburgh, Pennsylvania, United States of America.

Mallory D Witt (MD)

Department of Medicine, Los Angeles Biomedical Research Institute at Harbor-University of California Los Angeles, Torrance, California, United States of America.

Howard N Hodis (HN)

Atherosclerosis Research Unit, Keck School of Medicine at University of Southern California, Los Angeles, California, United States of America.

Russell P Tracy (RP)

Departments of Pathology & Laboratory Medicine, and Biochemistry, University of Vermont, Larner College of Medicine, Colchester, Vermont, United States of America.

Wendy S Post (WS)

Division of Cardiology, Johns Hopkins School of Medicine, Baltimore, Maryland, United States of America.
Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland, United States of America.

Sabina A Haberlen (SA)

Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland, United States of America.
ORCID: 0000-0002-9467-3454

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