Monocyte Dysfunction, Activation, and Inflammation After Long-Term Antiretroviral Therapy in an African Cohort.


Journal

The Journal of infectious diseases
ISSN: 1537-6613
Titre abrégé: J Infect Dis
Pays: United States
ID NLM: 0413675

Informations de publication

Date de publication:
26 09 2019
Historique:
received: 20 03 2019
accepted: 03 07 2019
pubmed: 20 7 2019
medline: 20 5 2020
entrez: 20 7 2019
Statut: ppublish

Résumé

Monocyte dysfunction may persist during antiretroviral therapy (ART). Frozen peripheral blood mononuclear cells of 30 human immunodeficiency virus (HIV)-infected ART-treated adults with sustained viral suppression and CD4 counts ≥500 cells/µL were consecutively analyzed for monocyte phenotypes and function. Nonclassical monocytes (CD14+, CD16++), interleukin (IL)-1β production, and expression of CD40 and CD86 were lower among ART-treated HIV-infected adults relative to age-matched HIV-negative adults (P = .01, P = .01, and P = .02, respectively). Intestinal fatty acid-binding protein, IL6, and soluble CD14 were higher among HIV-infected adults relative to HIV-negative adults (P = .0002, P = .04, and P = .0017, respectively). Further investigation is required to understand drivers of persistent monocyte activation and dysfunction.

Sections du résumé

BACKGROUND
Monocyte dysfunction may persist during antiretroviral therapy (ART).
METHODS
Frozen peripheral blood mononuclear cells of 30 human immunodeficiency virus (HIV)-infected ART-treated adults with sustained viral suppression and CD4 counts ≥500 cells/µL were consecutively analyzed for monocyte phenotypes and function.
RESULTS
Nonclassical monocytes (CD14+, CD16++), interleukin (IL)-1β production, and expression of CD40 and CD86 were lower among ART-treated HIV-infected adults relative to age-matched HIV-negative adults (P = .01, P = .01, and P = .02, respectively). Intestinal fatty acid-binding protein, IL6, and soluble CD14 were higher among HIV-infected adults relative to HIV-negative adults (P = .0002, P = .04, and P = .0017, respectively).
CONCLUSIONS
Further investigation is required to understand drivers of persistent monocyte activation and dysfunction.

Identifiants

pubmed: 31323092
pii: 5536380
doi: 10.1093/infdis/jiz320
pmc: PMC6761975
doi:

Substances chimiques

Anti-Retroviral Agents 0
Antigens, CD 0

Types de publication

Comparative Study Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

1414-1419

Subventions

Organisme : Wellcome Trust
ID : 107743/Z/15/Z
Pays : United Kingdom

Informations de copyright

© The Author(s) 2019. Published by Oxford University Press for the Infectious Diseases Society of America.

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Auteurs

Rose Nabatanzi (R)

Department of Immunology and Molecular Biology, Makerere University College of Health Sciences, Kampala, Uganda.

Lois Bayigga (L)

Department of Immunology and Molecular Biology, Makerere University College of Health Sciences, Kampala, Uganda.

Stephen Cose (S)

Medical Research Council/Uganda Virus Research Institute, Uganda Research Unit on AIDS, Entebbe, Uganda.

Sarah Rowland Jones (S)

Nuffield Department of Medicine, University of Oxford, United Kingdom.

Moses Joloba (M)

Department of Immunology and Molecular Biology, Makerere University College of Health Sciences, Kampala, Uganda.

Glenda Canderan (G)

Department of Pathology, Case Western Reserve University, Cleveland, Ohio.

Damalie Nakanjako (D)

Department of Medicine, Makerere University College of Health Sciences, Kampala, Uganda.
Infectious Diseases Institute, School of Medicine, Makerere University College of Health Sciences, Kampala, Uganda.

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Classifications MeSH