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Reversing Post-Infectious Epigenetic-Mediated Immune Suppression.

Abhimanyu1, Carlos O Ontiveros2,3, Rosa S Guerra-Resendez4

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Persistent epigenetic scars after infections cause long-term immune suppression and increased mortality. Research shows modulating specific pathways or using epigenetic drugs can reverse these detrimental scars, restoring immune function.

Keywords:
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Area of Science:

  • Immunology
  • Epigenetics
  • Infectious Diseases

Background:

  • The immune system balances pro-inflammatory and anti-inflammatory responses to manage infections and tissue repair.
  • Epigenetic mechanisms are crucial for regulating this balance, preventing excessive host tissue damage during severe or chronic infections.
  • Following treatment for infections like sepsis, pneumonia, hepatitis, HIV, TB, or schistosomiasis, detrimental epigenetic changes can lead to persistent immune suppression.

Purpose of the Study:

  • To investigate the role of epigenetic scars in long-lasting immune suppression after infection.
  • To identify mechanisms that induce and potentially reverse these detrimental epigenetic changes.
  • To explore therapeutic strategies for restoring immune function in infection survivors.

Main Methods:

  • Demonstration of epigenetic immune suppression mechanisms in vitro and in animal models.
  • Modulation of key signaling pathways including AMP-activated protein kinase (AMPK)-mammalian target of rapamycin (mTOR), nuclear factor of activated T cells (NFAT), and nuclear receptor (NR4A).
  • Utilizing drugs targeting epigenetic enzymes such as histone deacetylase (HDAC) inhibitors, DNA hypomethylating agents, and modifiers of the Nucleosome Remodeling and DNA methylation (NuRD) or Polycomb Repressive Complex (PRC).

Main Results:

  • Specific pathway modulations (AMPK-mTOR, NFAT, NR4A) were shown to block or reverse detrimental epigenetic scars.
  • Epigenetic drugs (HDAC inhibitors, DNA hypomethylating agents, NuRD/PRC modifiers) restored host immunity in models of sepsis, viral infection, and cancer.
  • Bioengineering approaches to reverse epigenetic marks or modify epigenetic enzymes/transcription factors also showed promise in preclinical models.

Conclusions:

  • Detrimental epigenetic scars persist after infection treatment, contributing to immune suppression and increased mortality.
  • Targeting specific molecular pathways, employing epigenetic drugs, or utilizing bioengineering strategies can reverse these scars.
  • Further translational studies are necessary to evaluate the clinical applicability of these approaches for restoring immune function in patients.