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Mitochondrial DAMPs induce endotoxin tolerance in human monocytes: an observation in patients with myocardial

Irene Fernández-Ruiz1, Francisco Arnalich2, Carolina Cubillos-Zapata1

  • 1Tumor Immunology Lab, IdiPAZ, Hospital La Paz, Madrid, Spain; Innate Immunity Group, IdiPAZ, La Paz Hospital, Madrid, Spain.

Plos One
|May 7, 2014
PubMed

Insights

Mitochondrial DNA (mtDNA) exposure causes endotoxin tolerance in monocytes, reducing cytokine production. High mtDNA levels in myocardial infarction patients correlate with this tolerance and increased infection risk.

Area of Science:

  • Immunology
  • Molecular Biology
  • Pathology

Background:

  • Monocyte exposure to mitochondrial Danger Associated Molecular Patterns (DAMPs), such as mitochondrial DNA (mtDNA), induces a refractory state to endotoxin stimulation.
  • This endotoxin tolerance (ET) is characterized by IRAK-M up-regulation, impaired p65 activity, and decreased cytokine production.

Purpose of the Study:

  • To investigate the role of circulating mtDNA in endotoxin tolerance.
  • To assess the correlation between mtDNA levels, ET status, and infection incidence in myocardial infarction (MI) patients.

Main Methods:

  • Isolation of monocytes and assessment of their response to endotoxin stimulation.
  • Quantification of circulating mitochondrial DNA (mtDNA) levels in patients.
  • Clinical observation of infection incidence in relation to ET status.

Main Results:

  • Monocytes from myocardial infarction (MI) patients showed elevated circulating mtDNA levels, correlating with endotoxin tolerance (ET).
  • Patients with a strong ET phenotype exhibited a higher incidence of infection.
  • Plasma mtDNA levels were associated with increased susceptibility to nosocomial infections.

Conclusions:

  • Circulating mitochondrial antigens, like plasma mtDNA, are linked to endotoxin tolerance.
  • Plasma mtDNA may serve as a useful biomarker for predicting infection susceptibility in MI and other tissue-damaging conditions.

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