Mitochondrial Network Fragmentation Leads to Dysfunction of Macrophages During Echinococcus multilocularis

Zihan Yang1,2,3,4, Yaogang Zhang5,6, Tao Zhang7

  • 1Research Center for High Altitude Medicine, Qinghai University, Xining 810000, China.

PubMed

Insights

Alveolar echinococcosis (AE) infection disrupts macrophage mitochondria, impairing immune response. Targeting mitochondrial fission could improve macrophage function and combat this parasitic disease.

Area of Science:

  • Immunology
  • Parasitology
  • Cell Biology

Background:

  • Alveolar echinococcosis (AE) is a severe liver disease caused by *Echinococcus multilocularis*.
  • Kupffer cells (macrophages in the liver) play a dual role in AE, offering protection but also aiding parasite immune escape in later stages.

Purpose of the Study:

  • To investigate the impact of *Echinococcus multilocularis* protoscoleces (PSCs) on macrophage mitochondrial morphology and function.
  • To assess the effects of PSCs infection on macrophage phagocytosis and apoptosis.
  • To explore the therapeutic potential of inhibiting mitochondrial fission in AE.

Main Methods:

  • Macrophages were infected with *Echinococcus multilocularis* protoscoleces (PSCs).
  • Mitochondrial morphology, membrane potential, reactive oxygen species (ROS) levels, and mitochondrial DNA (mtDNA) copy number were analyzed.
  • Macrophage phagocytic activity and apoptosis rates were measured.
  • The effect of inhibiting mitochondrial fission was evaluated.

Main Results:

  • PSCs infection led to mitochondrial network fragmentation, reduced membrane potential, increased ROS, and decreased mtDNA copy number in macrophages.
  • These mitochondrial changes promoted macrophage apoptosis and impaired their phagocytic function.
  • Inhibiting mitochondrial fission reversed mitochondrial dysfunction, reduced apoptosis, and enhanced phagocytosis.

Conclusions:

  • *Echinococcus multilocularis* protoscoleces disrupt macrophage mitochondria, contributing to immune evasion in alveolar echinococcosis.
  • Targeting mitochondrial fission presents a promising strategy to restore macrophage function and treat AE.

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