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In Vitro and In Vivo Detection of Mitophagy in Human Cells, C. Elegans, and Mice
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Gonococcal OMVs induce epithelial cell mitophagy in a dual PorB-dependent manner to enhance intracellular survival

Shuai Gao1, Stijn van der Veen1,2

  • 1Department of Microbiology, and Department of Dermatology of Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, People's Republic of China.

Autophagy
|May 18, 2024
PubMed

Insights

Neisseria gonorrhoeae outer membrane vesicles induce mitophagy in epithelial cells via a dual PorB-dependent pathway. This process enhances bacterial survival by reducing harmful reactive oxygen species.

Area of Science:

  • Microbiology
  • Cell Biology
  • Immunology

Background:

  • Outer membrane vesicles (OMVs) are secreted by Gram-negative bacteria for communication and environmental modulation.
  • Neisseria gonorrhoeae OMVs interact with epithelial cells, but their beneficial functions remain largely unexplored.
  • Understanding OMV functions is crucial for host-microbe interaction studies.

Purpose of the Study:

  • To investigate the functional activities of Neisseria gonorrhoeae OMVs during epithelial cell interactions.
  • To elucidate the mechanisms by which gonococcal OMVs influence host cell processes.
  • To determine how OMV-induced cellular changes impact bacterial survival.

Main Methods:

  • Endocytosis of gonococcal OMVs by epithelial cells.
  • Analysis of mitophagy induction via PorB-dependent pathways.
  • Investigation of PINK1, OPTN, CALCOCO2/NDP52, and SQSTM1/p62 involvement.
  • Assessment of mitochondrial membrane potential and reactive oxygen species production.
  • Role of E3 ubiquitin ligase RNF213 in PorB ubiquitination.

Main Results:

  • Gonococcal OMVs are endocytosed by epithelial cells.
  • OMVs induce mitophagy through two distinct PorB-dependent mechanisms.
  • PorB translocates to mitochondria, dissipating membrane potential and initiating PINK1/OPTN/CALCOCO2/NDP52-mediated mitophagy.
  • PorB undergoes K63-linked polyubiquitination at K171 by RNF213, activating an SQSTM1/p62-dependent mitophagy pathway.
  • Mitophagy induction reduces bactericidal mitochondrial reactive oxygen species, favoring intracellular bacterial survival.

Conclusions:

  • Neisseria gonorrhoeae utilizes a sophisticated bimodal OMV-mediated mechanism to manipulate host mitophagy.
  • The PorB protein is central to initiating distinct mitophagy pathways.
  • This OMV-induced mitophagy enhances gonococcal survival within the intracellular niche by mitigating host defense mechanisms.
Keywords:
MitophagyNeisseria gonorrhoeaePorBRNF213outer membrane vesiclespolyubiquitination

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