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Listeria hijacks host mitophagy through a novel mitophagy receptor to evade killing

Yifan Zhang1, Yikun Yao1, Xiaoxu Qiu1

  • 1CAS Key Laboratory of Tissue Microenvironment and Tumor, CAS Center for Excellence in Molecular Cell Science, Shanghai Institute of Nutrition and Health, Shanghai Institutes for Biological Sciences, University of the Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai, China.

Nature Immunology
|February 27, 2019
PubMed

Insights

The bacterium Listeria monocytogenes triggers mitophagy, a cellular cleaning process, to survive within host cells. This pathogen hijacks the NLRX1 protein to induce mitophagy, evading immune defenses.

Area of Science:

  • Cellular Biology
  • Immunology
  • Microbiology

Background:

  • Mitophagy is a crucial cellular process for removing damaged mitochondria and maintaining cellular homeostasis.
  • Intracellular pathogens have evolved diverse mechanisms to evade host immune responses and ensure their survival.
  • Mitochondria play a significant role in cellular immunity and pathogen defense.

Purpose of the Study:

  • To investigate the role of mitophagy in Listeria monocytogenes infection.
  • To identify host factors involved in L. monocytogenes-induced mitophagy.
  • To elucidate the mechanism by which L. monocytogenes exploits host mitophagy for survival.

Main Methods:

  • Macrophage cell culture and infection with L. monocytogenes.
  • Western blotting and immunoprecipitation to detect protein interactions.
  • Mitochondrial reactive oxygen species (ROS) measurement.
  • NLRX1 knockout and knockdown experiments.
  • Mitophagy inhibition using pharmacological agents.

Main Results:

  • L. monocytogenes infection induces mitophagy in macrophages, dependent on the virulence factor listeriolysin O (LLO).
  • NLRX1, a mitochondrial-localized Nod-like receptor, directly interacts with LC3 via its LC3-interacting region (LIR) motif.
  • NLRX1 and its LIR motif are essential for L. monocytogenes-induced mitophagy.
  • NLRX1 deficiency or mitophagy inhibition enhances mitochondrial ROS production, suppressing L. monocytogenes survival.
  • LLO induces NLRX1 oligomerization, promoting its interaction with LC3 and subsequent mitophagy.

Conclusions:

  • L. monocytogenes exploits host mitophagy as a survival strategy by hijacking the NLRX1 receptor.
  • NLRX1 acts as a novel mitophagy receptor, mediating the clearance of mitochondria during bacterial infection.
  • Targeting NLRX1-mediated mitophagy presents a potential therapeutic strategy to combat L. monocytogenes infections.

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