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High-Resolution Fluorespirometry to Assess Dynamic Changes in Mitochondrial Membrane Potential in Human Immune Cells
Published on: May 24, 2024
Short communication: decrease in mitochondrial transmembrane potential in peripheral blood mononuclear cells of
Jan B Groener1, Ulrich Seybold, Thomas Vollbrecht
1Division of Infectious Diseases, Medizinische Poliklinik-Innenstadt, University of Munich, Germany.
AIDS Research and Human Retroviruses
|February 15, 2011
Summary
HIV postexposure prophylaxis (PEP) using emtricitabine/tenofovir and lopinavir/ritonavir temporarily reduced mitochondrial function in healthy individuals. Mitochondrial transmembrane potential (ΔΨm) returned to normal after discontinuing antiretroviral therapy.
Area of Science:
- Immunology
- Pharmacology
- Cell Biology
Background:
- Mitochondrial dysfunction is a potential concern with antiretroviral drugs.
- Understanding the impact of HIV postexposure prophylaxis (PEP) on cellular health is crucial.
Purpose of the Study:
- To investigate the effects of a 4-week HIV-PEP regimen on mitochondrial transmembrane potential (ΔΨm) in peripheral blood mononuclear cells (PBMCs).
- To assess whether HIV-PEP influences apoptosis rates in PBMCs.
Main Methods:
- Peripheral blood mononuclear cells (PBMCs) were collected from 18 HIV-uninfected individuals undergoing HIV-PEP.
- Mitochondrial transmembrane potential (ΔΨm) was measured using JC-1 staining and FACS analysis.
- Apoptosis was evaluated via Annexin-V-FITC and propidium iodide staining.
- Statistical analysis employed mixed effects regression models.
Main Results:
- A significant decrease in ΔΨm was observed during the 4-week HIV-PEP course (p=0.0015 linear, p=0.0039 quadratic).
- ΔΨm levels normalized several weeks after cessation of antiretroviral treatment.
- No significant changes in apoptosis rates were detected (p=0.42).
Conclusions:
- HIV-PEP with emtricitabine/tenofovir and lopinavir/ritonavir can lead to temporary mitochondrial dysfunction.
- The observed mitochondrial dysfunction during HIV-PEP does not appear to induce significant apoptosis.
- Emerging antiretrovirals like tenofovir and emtricitabine may carry risks associated with mitochondrial side effects.
