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Front Immunol. 2019 Apr 16;10:785. doi: 10.3389/fimmu.2019.00785. eCollection 2019.

Altered Lipidome Composition Is Related to Markers of Monocyte and Immune Activation in Antiretroviral Therapy Treated Human Immunodeficiency Virus (HIV) Infection and in Uninfected Persons.

Author information

1
Division of Medical Laboratory Science, School of Health and Rehabilitation Sciences, Ohio State University, Columbus, OH, United States.
2
Personalized Food and Nutritional Metabolomics for Health Discovery Theme, The Ohio State University, Columbus, OH, United States.
3
Department of Human Sciences, Ohio State University, Columbus, OH, United States.
4
Division of Infectious Diseases, Department of Medicine, The University of Texas Health Science Center, Houston, TX, United States.
5
Department of Population and Quantitative Health Sciences, Case Western Reserve University, Cleveland, OH, United States.
6
Department of Nutrition, Case Western Reserve University, Cleveland, OH, United States.
7
Division of Infectious Diseases, Department of Medicine, Ohio State University, Columbus, OH, United States.
8
Division of Infectious Diseases, Department of Internal Medicine, Case Western Reserve University/University Hospitals of Cleveland, Cleveland, OH, United States.

Abstract

Background: HIV infection and antiretroviral therapy (ART) have both been linked to dyslipidemia and increased cardiovascular disease (CVD) risk. Alterations in the composition of saturated (SaFA), monounsaturated (MUFA), and polyunsaturated (PUFA) fatty acids are related to inflammation and CVD progression in HIV-uninfected (HIV-) populations. The relationships among the lipidome and markers of monocyte and immune activation in HIV-infected (HIV+) individuals are not well understood. Methods: Concentrations of serum lipids and their fatty acid composition were measured by direct infusion-tandem mass spectrometry in samples from 20 ART-treated HIV+ individuals and 20 HIV- individuals. Results: HIV+ individuals had increased levels of free fatty acids (FFAs) with enrichment of SaFAs, including palmitic acid (16:0) and stearic acid (18:0), and these levels were directly associated with markers of monocyte (CD40, HLA-DR, TLR4, CD36) and serum inflammation (LBP, CRP). PUFA levels were reduced significantly in HIV+ individuals, and many individual PUFA species levels were inversely related to markers of monocyte activation, such as tissue factor, TLR4, CD69, and SR-A. Also in HIV+ individuals, the composition of lysophosphatidylcholine (LPC) was enriched for SaFAs; LPC species containing SaFAs were directly associated with IL-6 levels and monocyte activation. We similarly observed direct relationships between levels of SaFAs and inflammation in HIV uninfected individuals. Further, SaFA exposure altered monocyte subset phenotypes and inflammatory cytokine production in vitro. Conclusions: The lipidome is altered in ART-treated HIV infection, and may contribute to inflammation and CVD progression. Detailed lipidomic analyses may better assess CVD risk in both HIV+ and HIV- individuals than does traditional lipid profiling.

KEYWORDS:

HIV; cardiovascular disease; free fatty acids; inflammation; lipidome; monocytes

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