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TNF promotes M1 polarization through mitochondrial metabolism in injured spinal cord

Sen Lin1, Zipeng Zhou1, Haosen Zhao1

  • 1Department of Orthopedic, First Affiliated Hospital of Jinzhou Medical University, Jinzhou, PR China.

Free Radical Biology & Medicine
|July 12, 2021
PubMed

Insights

Removing tumor necrosis factor (TNF) promotes beneficial M2 macrophage/microglia (M/Ms) phenotypes and improves mitochondrial function, aiding spinal cord injury (SCI) recovery. This suggests TNF is a potential therapeutic target for SCI.

Area of Science:

  • Neuroscience
  • Immunology
  • Cell Biology

Background:

  • Macrophages and microglia (M/Ms) adopt a detrimental M1 neurotoxic phenotype post-spinal cord injury (SCI), hindering repair.
  • Tumor necrosis factor (TNF) is known to promote the M1 polarization of M/Ms in various conditions.

Purpose of the Study:

  • To investigate the role of TNF in M/M polarization and mitochondrial metabolism following SCI.
  • To evaluate the therapeutic potential of TNF modulation for SCI recovery.

Main Methods:

  • Studied M/M phenotype conversion (M1 to M2) in TNF-ablated models (in vivo and in vitro).
  • Assessed mitochondrial metabolism, reactive oxygen species (ROS) activity, and M1-specific gene expression.
  • Compared TNF ablation effects with N-Acetyl-l-cysteine (NAC) and TPEN treatments.

Main Results:

  • TNF ablation promoted a shift from M1 to M2 M/M phenotypes and enhanced mitochondrial metabolism.
  • Reduced ROS activity and M1 marker expression were observed in TNF-null conditions, linked to PGC-1α accumulation.
  • Absence of TNF improved mitochondrial morphology and quantity, facilitating a faster M2 switch compared to NAC.

Conclusions:

  • Sustained TNF expression is detrimental to spinal cord injury recovery.
  • Targeting TNF offers significant potential for immunomodulatory treatment strategies in SCI.
Keywords:
MitochondriaRedox imbalanceSpinal cord injuryTNFZinc

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