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Avian Pathogenic Escherichia coli T6SS Effector Protein Hcp2 Induces Mitochondrial Dysfunction and Activates

Bingyu Zhao1,2, Ziqi Li1,2, Liyang Dai1,2

  • 1Anhui Province Key Laboratory of Veterinary Pathobiology and Disease Control, College of Veterinary Medicine, Anhui Agricultural University, Hefei, 230036, China, ahau.edu.cn.

Transboundary and Emerging Diseases
|June 25, 2026
PubMed

Insights

Avian pathogenic E. coli Hcp2 protein disrupts mitochondrial function and triggers mitophagy in chicken cells. This study reveals a novel mechanism of host cell damage by Hcp2, impacting cellular homeostasis.

Area of Science:

  • Microbiology
  • Cell Biology
  • Pathogenesis

Background:

  • Avian pathogenic Escherichia coli (APEC) utilizes secretion systems for host colonization and invasion.
  • The type VI secretion system (T6SS) component, hemolysin-coregulatory protein (Hcp), acts as both a structural element and a virulence effector.
  • The precise pathogenic mechanisms of Hcp2 impacting host cell function are not fully elucidated.

Purpose of the Study:

  • To investigate the effect of Hcp2 on mitochondrial function in chicken tracheal mucosal epithelial (CTE) cells.
  • To elucidate the role of Hcp2 in APEC-induced host cell damage.
  • To understand the cellular response, specifically mitophagy, to Hcp2-induced mitochondrial dysfunction.

Main Methods:

  • Exposure of CTE cells to purified Hcp2 protein.
  • Assessment of mitochondrial function via reactive oxygen species (ROS) levels, mitochondrial membrane potential, and intracellular calcium.
  • Analysis of mitophagy using transmission electron microscopy (TEM), immunofluorescence microscopy, Western blotting (LC3-I/II, p62/SQSTM1), and co-localization studies.

Main Results:

  • Hcp2 exposure caused significant mitochondrial dysfunction, including increased ROS, membrane depolarization, and calcium overload.
  • Hcp2 disrupted cellular homeostasis, indicating mitochondrial oxidative stress.
  • Evidence of mitophagy activation, including autophagosome formation, increased LC3-II conversion, altered p62 levels, and degradation of mitochondrial proteins.

Conclusions:

  • Hcp2 disrupts mitochondrial functional homeostasis in CTE cells.
  • Hcp2 triggers mitophagy as a cellular response to mitochondrial damage.
  • This study reveals a novel pathogenic mechanism involving Hcp2-mediated mitochondrial dysfunction and mitophagy activation in APEC infection.
Keywords:
avian pathogenic Escherichia colihemolysin-coregulatory protein 2mitochondrial dysfunctionmitophagytype VI secretion system

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