Plasma cholesterol efflux capacity from human THP-1 macrophages is reduced in HIV-infected patients: impact of HAART.

Petra El Khoury, Mathilde Ghislain, Elise F Villard, Wilfried Le Goff, Caroline Lascoux-Combe, Patrick Yeni, Laurence Meyer, Corinne Vigouroux, Cécile Goujard, Maryse Guerin

Journal: Journal of lipid research 2015;56(3):692-702

PMID: 25573889

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Abstract

The capacity of HDL to remove cholesterol from macrophages is inversely associated with the severity of angiographic coronary artery disease. The effect of human immunodeficiency virus (HIV) infection or its treatment on the ability of HDL particles to stimulate cholesterol efflux from human macrophages has never been studied. We evaluated the capacity of whole plasma and isolated HDL particles from HIV-infected subjects (n = 231) and uninfected controls (n = 200), as well as in a subset of 41 HIV subjects receiving highly active antiretroviral therapy (HAART) to mediate cholesterol efflux from human macrophages. Plasma cholesterol efflux capacity was reduced (-12%; P = 0.001) in HIV patients as compared with controls. HIV infection reduced by 27% (P < 0.05) the capacity of HDL subfractions to promote cholesterol efflux from macrophages. We observed a reduced ABCA1-dependent efflux capacity of plasma (-27%; P < 0.0001) from HIV-infected subjects as a result of a reduction in the efflux capacity of HDL3 particles. HAART administration restored the capacity of plasma from HIV patients to stimulate cholesterol efflux from human macrophages (9.4%; P = 0.04). During HIV infection, the capacity of whole plasma to remove cholesterol from macrophages is reduced, thus potentially contributing to the increased coronary heart disease in the HIV population. HAART administration restored the removal of cholesterol from macrophages by increasing HDL functionality.

Address: Institut National de la Santé et de la Recherche Médicale (INSERM) UMRS1166, Hôpital de la Pitié, Paris, France; Sorbonne Universités, UMPC Univ Paris 6, Paris, France; Université Saint Joseph, Faculté de pharmacie, Beyrouth, Liban.; INSERM, UMRS 1018, CESP, Le Kremlin-Bicêtre, France; Service d'Epidémiologie et de Santé Publique, Hôpital Bicêtre, Assistance Publique-Hôpitaux de Paris (AP-HP), Le Kremlin-Bicêtre, France.; Institut National de la Santé et de la Recherche Médicale (INSERM) UMRS1166, Hôpital de la Pitié, Paris, France; Sorbonne Universités, UMPC Univ Paris 6, Paris, France.; Institut National de la Santé et de la Recherche Médicale (INSERM) UMRS1166, Hôpital de la Pitié, Paris, France; Sorbonne Universités, UMPC Univ Paris 6, Paris, France; ICAN Institute of Cardiometabolism and Nutrition, Hôpital de la Pitié, Paris, France.; Service de Maladies Infectieuses, Hôpital Saint-Louis, AP-HP, Paris, France.; Service de Maladies Infectieuses, Hôpital Bichat, AP-HP, Paris, France.; INSERM, UMRS 1018, CESP, Le Kremlin-Bicêtre, France; Service d'Epidémiologie et de Santé Publique, Hôpital Bicêtre, Assistance Publique-Hôpitaux de Paris (AP-HP), Le Kremlin-Bicêtre, France; Université Paris-Sud, Le Kremlin-Bicêtre, France.; Sorbonne Universités, UMPC Univ Paris 6, Paris, France; ICAN Institute of Cardiometabolism and Nutrition, Hôpital de la Pitié, Paris, France; Assistance Publique-Hôpitaux de Paris, Hôpital Saint-Antoine, Laboratoire de Biologie et Génétique Moléculaires, Paris, France; INSERM UMRS938, Centre de recherche Saint-Antoine, Paris, France.; INSERM, UMRS 1018, CESP, Le Kremlin-Bicêtre, France; Université Paris-Sud, Le Kremlin-Bicêtre, France; Service de Médecine Interne, Hôpital Bicêtre, AP-HP, Le Kremlin-Bicêtre, France.; Institut National de la Santé et de la Recherche Médicale (INSERM) UMRS1166, Hôpital de la Pitié, Paris, France; Sorbonne Universités, UMPC Univ Paris 6, Paris, France; ICAN Institute of Cardiometabolism and Nutrition, Hôpital de la Pitié, Paris, France. Electronic address: [email protected].

DOI: 10.1194/jlr.M054510

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MeSH Terms: ATP Binding Cassette Transporter 1, Adult, Antiretroviral Therapy, Highly Active, Cell Line, Tumor, Cholesterol, Female, HIV Infections, Humans, Lipoproteins, HDL3, Macrophages, Male, Middle Aged