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Inhibitory effects of mitochondrial metabolic inhibitors on interferon action

W J Richtsmeier1, S E Grossberg

  • 1Department of Microbiology, Medical College of Wisconsin, Milwaukee 53226.

Journal of Interferon Research
|February 1, 1989
PubMed

Insights

Mitochondrial function is crucial for the antiviral activity of interferons (IFNs). Inhibiting mitochondrial processes with antimetabolites significantly suppressed the effectiveness of IFNs, highlighting their importance in cellular defense.

Area of Science:

  • Cellular and Molecular Biology
  • Immunology
  • Virology

Background:

  • Interferons (IFNs) are key cytokines mediating antiviral responses.
  • The precise cellular mechanisms regulating IFN antiviral action are not fully elucidated.
  • Previous studies suggested cytoplasmic protein synthesis is essential for IFN efficacy.

Purpose of the Study:

  • To investigate the role of mitochondrial functions in the antiviral action of human interferons (HuIFN-alpha and HuIFN-gamma).
  • To determine if inhibiting mitochondrial processes affects IFN-mediated antiviral effects.

Main Methods:

  • Human cells and mouse L cells were treated with various antimetabolites targeting mitochondrial functions.
  • Inhibitors included cycloheximide (cytoplasmic protein synthesis inhibitor), chloramphenicol (mitochondrial protein synthesis inhibitor), oligomycin (oxidative phosphorylation inhibitor), and dinitrophenol/1799 (uncouplers).
  • The antiviral effect of IFNs was assessed in treated and untreated cells.

Main Results:

  • Cycloheximide partially inhibited IFN antiviral action, while chloramphenicol showed significant suppression at high concentrations.
  • Combined cycloheximide and chloramphenicol treatments resulted in greater inhibition of IFN antiviral effects.
  • Inhibitors of oxidative phosphorylation (oligomycin, dinitrophenol, 1799) also suppressed IFN antiviral activity.
  • Similar results were observed with mouse IFNs in mouse cells.

Conclusions:

  • Intact mitochondrial functions are essential for the full expression of antiviral actions mediated by IFN-alpha and IFN-gamma.
  • Mitochondria play a critical, previously underestimated role in the cellular response to viral infections via IFNs.

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