Biomarkers of Microbial Translocation and Macrophage Activation: Association With Progression of Subclinical Atherosclerosis in HIV-1 Infection
Background. The relationships between soluble CD 14 (sCD14), endotoxin (lipopolysaccharide [LPS]), and progression of atherosclerosis have not been defined in human immunodeficiency virus (HIV) infection. Methods. We retrospectively assessed serum sCD14 and LPS levels of 91 subjects in a prospective...
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| Published in | The Journal of infectious diseases Vol. 206; no. 10; pp. 1558 - 1567 |
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| Main Authors | , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Oxford
Oxford University Press
15.11.2012
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| Subjects | |
| Online Access | Get full text |
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| Abstract | Background. The relationships between soluble CD 14 (sCD14), endotoxin (lipopolysaccharide [LPS]), and progression of atherosclerosis have not been defined in human immunodeficiency virus (HIV) infection. Methods. We retrospectively assessed serum sCD14 and LPS levels of 91 subjects in a prospective 3-year study of carotid artery intima-media thickness (CIMT) (AIDS Clinical Trials Group [ACTG] 5078), where subjects were enrolled as risk factor-controlled triads of HIV-uninfected (n = 36) and HIV-infected individuals with (n = 29) or without (n = 26) protease inhibitor (PI)-based therapy for ≥2 years. The primary end point was the yearly rate of change of CIMT (∆CIMT). Results. In multivariate analysis of the HIV-infected subjects, each 1 μg/mL above the mean of baseline serum sCD14 corresponded to an additional 1.52 μm/y (95% confidence interval, .07-2.98; P= .04) in the ∆CIMT. Every 100 pg/mL above the mean of baseline serum LPS corresponded to an additional 0.49 μm/y (95% confidence interval, .18–. 81; P =. 003) in the ∆CIMT. However, in univariate analysis in the HIV-uninfected group sCD14 (P = .33) and LPS (P = .27) levels were not associated with higher ∆CIMT. HIV infection and PI therapy were not associated with baseline serum LPS and sCD14 levels (P > .1). Conclusions. Our data are among the first to suggest that serum biomarkers of microbial translocation (LPS) and macrophage activation (sCD14) predict subclinical atherosclerosis progression in HIV-infected persons. |
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| AbstractList | Background. The relationships between soluble CD 14 (sCD14), endotoxin (lipopolysaccharide [LPS]), and progression of atherosclerosis have not been defined in human immunodeficiency virus (HIV) infection. Methods. We retrospectively assessed serum sCD14 and LPS levels of 91 subjects in a prospective 3-year study of carotid artery intima-media thickness (CIMT) (AIDS Clinical Trials Group [ACTG] 5078), where subjects were enrolled as risk factor-controlled triads of HIV-uninfected (n = 36) and HIV-infected individuals with (n = 29) or without (n = 26) protease inhibitor (PI)-based therapy for ≥2 years. The primary end point was the yearly rate of change of CIMT (∆CIMT). Results. In multivariate analysis of the HIV-infected subjects, each 1 μg/mL above the mean of baseline serum sCD14 corresponded to an additional 1.52 μm/y (95% confidence interval, .07-2.98; P= .04) in the ∆CIMT. Every 100 pg/mL above the mean of baseline serum LPS corresponded to an additional 0.49 μm/y (95% confidence interval, .18–. 81; P =. 003) in the ∆CIMT. However, in univariate analysis in the HIV-uninfected group sCD14 (P = .33) and LPS (P = .27) levels were not associated with higher ∆CIMT. HIV infection and PI therapy were not associated with baseline serum LPS and sCD14 levels (P > .1). Conclusions. Our data are among the first to suggest that serum biomarkers of microbial translocation (LPS) and macrophage activation (sCD14) predict subclinical atherosclerosis progression in HIV-infected persons. Background. The relationships between soluble CD14 (sCD14), endotoxin (lipopolysaccharide [LPS]), and progression of atherosclerosis have not been defined in human immunodeficiency virus (HIV) infection. Methods. We retrospectively assessed serum sCD14 and LPS levels of 91 subjects in a prospective 3-year study of carotid artery intima-media thickness (CIMT) (AIDS Clinical Trials Group [ACTG] 5078), where subjects were enrolled as risk factor–controlled triads of HIV-uninfected (n = 36) and HIV-infected individuals with (n = 29) or without (n = 26) protease inhibitor (PI)–based therapy for ≥2 years. The primary end point was the yearly rate of change of CIMT (ΔCIMT). Results. In multivariate analysis of the HIV-infected subjects, each 1 µg/mL above the mean of baseline serum sCD14 corresponded to an additional 1.52 µm/y (95% confidence interval, .07–2.98; P = .04) in the ΔCIMT. Every 100 pg/mL above the mean of baseline serum LPS corresponded to an additional 0.49 µm/y (95% confidence interval, .18–.81; P = .003) in the ΔCIMT. However, in univariate analysis in the HIV-uninfected group sCD14 ( P = .33) and LPS ( P = .27) levels were not associated with higher ΔCIMT. HIV infection and PI therapy were not associated with baseline serum LPS and sCD14 levels ( P > .1). Conclusions. Our data are among the first to suggest that serum biomarkers of microbial translocation (LPS) and macrophage activation (sCD14) predict subclinical atherosclerosis progression in HIV-infected persons. The relationships between soluble CD14 (sCD14), endotoxin (lipopolysaccharide [LPS]), and progression of atherosclerosis have not been defined in human immunodeficiency virus (HIV) infection. We retrospectively assessed serum sCD14 and LPS levels of 91 subjects in a prospective 3-year study of carotid artery intima-media thickness (CIMT) (AIDS Clinical Trials Group [ACTG] 5078), where subjects were enrolled as risk factor-controlled triads of HIV-uninfected (n = 36) and HIV-infected individuals with (n = 29) or without (n = 26) protease inhibitor (PI)-based therapy for ≥2 years. The primary end point was the yearly rate of change of CIMT (ΔCIMT). In multivariate analysis of the HIV-infected subjects, each 1 µg/mL above the mean of baseline serum sCD14 corresponded to an additional 1.52 µm/y (95% confidence interval, .07-2.98; P = .04) in the ΔCIMT. Every 100 pg/mL above the mean of baseline serum LPS corresponded to an additional 0.49 µm/y (95% confidence interval, .18-.81; P = .003) in the ΔCIMT. However, in univariate analysis in the HIV-uninfected group sCD14 (P = .33) and LPS (P = .27) levels were not associated with higher ΔCIMT. HIV infection and PI therapy were not associated with baseline serum LPS and sCD14 levels (P > .1). Our data are among the first to suggest that serum biomarkers of microbial translocation (LPS) and macrophage activation (sCD14) predict subclinical atherosclerosis progression in HIV-infected persons. The relationships between soluble CD14 (sCD14), endotoxin (lipopolysaccharide [LPS]), and progression of atherosclerosis have not been defined in human immunodeficiency virus (HIV) infection.BACKGROUNDThe relationships between soluble CD14 (sCD14), endotoxin (lipopolysaccharide [LPS]), and progression of atherosclerosis have not been defined in human immunodeficiency virus (HIV) infection.We retrospectively assessed serum sCD14 and LPS levels of 91 subjects in a prospective 3-year study of carotid artery intima-media thickness (CIMT) (AIDS Clinical Trials Group [ACTG] 5078), where subjects were enrolled as risk factor-controlled triads of HIV-uninfected (n = 36) and HIV-infected individuals with (n = 29) or without (n = 26) protease inhibitor (PI)-based therapy for ≥2 years. The primary end point was the yearly rate of change of CIMT (ΔCIMT).METHODSWe retrospectively assessed serum sCD14 and LPS levels of 91 subjects in a prospective 3-year study of carotid artery intima-media thickness (CIMT) (AIDS Clinical Trials Group [ACTG] 5078), where subjects were enrolled as risk factor-controlled triads of HIV-uninfected (n = 36) and HIV-infected individuals with (n = 29) or without (n = 26) protease inhibitor (PI)-based therapy for ≥2 years. The primary end point was the yearly rate of change of CIMT (ΔCIMT).In multivariate analysis of the HIV-infected subjects, each 1 µg/mL above the mean of baseline serum sCD14 corresponded to an additional 1.52 µm/y (95% confidence interval, .07-2.98; P = .04) in the ΔCIMT. Every 100 pg/mL above the mean of baseline serum LPS corresponded to an additional 0.49 µm/y (95% confidence interval, .18-.81; P = .003) in the ΔCIMT. However, in univariate analysis in the HIV-uninfected group sCD14 (P = .33) and LPS (P = .27) levels were not associated with higher ΔCIMT. HIV infection and PI therapy were not associated with baseline serum LPS and sCD14 levels (P > .1).RESULTSIn multivariate analysis of the HIV-infected subjects, each 1 µg/mL above the mean of baseline serum sCD14 corresponded to an additional 1.52 µm/y (95% confidence interval, .07-2.98; P = .04) in the ΔCIMT. Every 100 pg/mL above the mean of baseline serum LPS corresponded to an additional 0.49 µm/y (95% confidence interval, .18-.81; P = .003) in the ΔCIMT. However, in univariate analysis in the HIV-uninfected group sCD14 (P = .33) and LPS (P = .27) levels were not associated with higher ΔCIMT. HIV infection and PI therapy were not associated with baseline serum LPS and sCD14 levels (P > .1).Our data are among the first to suggest that serum biomarkers of microbial translocation (LPS) and macrophage activation (sCD14) predict subclinical atherosclerosis progression in HIV-infected persons.CONCLUSIONSOur data are among the first to suggest that serum biomarkers of microbial translocation (LPS) and macrophage activation (sCD14) predict subclinical atherosclerosis progression in HIV-infected persons. Background. The relationships between soluble CD14 (sCD14), endotoxin (lipopolysaccharide [LPS]), and progression of atherosclerosis have not been defined in human immunodeficiency virus (HIV) infection. Methods. We retrospectively assessed serum sCD14 and LPS levels of 91 subjects in a prospective 3-year study of carotid artery intima-media thickness (CIMT) (AIDS Clinical Trials Group [ACTG] 5078), where subjects were enrolled as risk factor-controlled triads of HIV-uninfected (n = 36) and HIV-infected individuals with (n = 29) or without (n = 26) protease inhibitor (PI)-based therapy for > or =2 years. The primary end point was the yearly rate of change of CIMT ([Delta]CIMT). Results. In multivariate analysis of the HIV-infected subjects, each 1 mu g/mL above the mean of baseline serum sCD14 corresponded to an additional 1.52 mu m/y (95% confidence interval, .07-2.98; P = .04) in the [Delta]CIMT. Every 100 pg/mL above the mean of baseline serum LPS corresponded to an additional 0.49 mu m/y (95% confidence interval, .18-.81; P = .003) in the [Delta]CIMT. However, in univariate analysis in the HIV-uninfected group sCD14 (P = .33) and LPS (P = .27) levels were not associated with higher [Delta]CIMT. HIV infection and PI therapy were not associated with baseline serum LPS and sCD14 levels (P > .1). Conclusions. Our data are among the first to suggest that serum biomarkers of microbial translocation (LPS) and macrophage activation (sCD14) predict subclinical atherosclerosis progression in HIV-infected persons. |
| Author | Yang, Otto O. Kelesidis, Theodoros Currier, Judith S. Hodis, Howard N. Kendall, Michelle A. |
| AuthorAffiliation | 4 Center for Biostatistics in AIDS Research 2 Department of Microbiology, Immunology, and Molecular Genetics , David Geffen School of Medicine, University of California 3 Atherosclerosis Research Unit, Department of Medicine and Preventive Medicine , Keck School of Medicine, University of Southern California , Los Angeles 1 Department of Medicine, Division of Infectious Diseases |
| AuthorAffiliation_xml | – name: 2 Department of Microbiology, Immunology, and Molecular Genetics , David Geffen School of Medicine, University of California – name: 1 Department of Medicine, Division of Infectious Diseases – name: 3 Atherosclerosis Research Unit, Department of Medicine and Preventive Medicine , Keck School of Medicine, University of Southern California , Los Angeles – name: 4 Center for Biostatistics in AIDS Research |
| Author_xml | – sequence: 1 givenname: Theodoros surname: Kelesidis fullname: Kelesidis, Theodoros – sequence: 2 givenname: Michelle A. surname: Kendall fullname: Kendall, Michelle A. – sequence: 3 givenname: Otto O. surname: Yang fullname: Yang, Otto O. – sequence: 4 givenname: Howard N. surname: Hodis fullname: Hodis, Howard N. – sequence: 5 givenname: Judith S. surname: Currier fullname: Currier, Judith S. |
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| ContentType | Journal Article |
| Copyright | Copyright © 2012 Oxford University Press on behalf of the Infectious Diseases Society of America 2015 INIST-CNRS The Author 2012. Published by Oxford University Press on behalf of the Infectious Diseases Society of America. All rights reserved. For Permissions, please e-mail: . 2012 |
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| Issue | 10 |
| Keywords | Immunopathology HIV-1 virus Retroviridae Biological marker Cardiovascular disease AIDS Immune deficiency Lentivirus Vascular disease Virus Infection Viral disease Atherosclerosis Human immunodeficiency virus Macrophage |
| Language | English |
| License | CC BY 4.0 |
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| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Presented in part: 19th Conference on Retroviruses and Opportunistic Infections (CROI 2012), Seattle, Washington, 5–8 March 2012. Abstract O-155. |
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| PublicationTitle | The Journal of infectious diseases |
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| Snippet | Background. The relationships between soluble CD 14 (sCD14), endotoxin (lipopolysaccharide [LPS]), and progression of atherosclerosis have not been defined in... The relationships between soluble CD14 (sCD14), endotoxin (lipopolysaccharide [LPS]), and progression of atherosclerosis have not been defined in human... Background. The relationships between soluble CD14 (sCD14), endotoxin (lipopolysaccharide [LPS]), and progression of atherosclerosis have not been defined in... Background. The relationships between soluble CD14 (sCD14), endotoxin (lipopolysaccharide [LPS]), and progression of atherosclerosis have not been defined in... |
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| SubjectTerms | Adult AIDS Anti-HIV Agents - therapeutic use Atherosclerosis Atherosclerosis - complications Bacterial Translocation Biological and medical sciences Biomarkers - blood Biomarkers - metabolism Body mass index Cholesterols Cohort Studies Female Fundamental and applied biological sciences. Psychology HDL lipoproteins HIV HIV infections HIV Infections - blood HIV Infections - complications HIV Infections - drug therapy HIV-1 HIV/AIDS Human immunodeficiency virus Human immunodeficiency virus 1 Human viral diseases Humans Infectious diseases Lipopolysaccharide Receptors - blood Lipopolysaccharide Receptors - metabolism Lipopolysaccharides - blood Lipopolysaccharides - metabolism Macrophage Activation - physiology Major and Brief Reports Male Medical sciences Memory interference Microbiology Middle Aged Miscellaneous Modeling Protease Inhibitors - therapeutic use Rates of change Retrospective Studies Viral diseases Viral diseases of the lymphoid tissue and the blood. Aids Virology |
| Title | Biomarkers of Microbial Translocation and Macrophage Activation: Association With Progression of Subclinical Atherosclerosis in HIV-1 Infection |
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