Autophagy and Intracellular Membrane Trafficking Subversion by Pathogenic Yersinia Species

Marion Lemarignier1,2, Javier Pizarro-Cerdá1,3,4,5

  • 1Yersinia Research Unit, Institut Pasteur, F-75015 Paris, France.

Biomolecules
|December 9, 2020
PubMed

Insights

Pathogenic Yersinia bacteria, including Yersinia pseudotuberculosis, Y. enterocolitica, and Y. pestis, hijack host cell autophagy for intracellular replication. This review explores these host-pathogen interactions in enteric yersiniosis and plague.

Area of Science:

  • Microbiology
  • Cell Biology
  • Immunology

Background:

  • Pathogenic Yersinia species (Yersinia pseudotuberculosis, Y. enterocolitica, Y. pestis) cause human diseases through extracellular growth.
  • These bacteria are known to invade, replicate, and survive within host cells.
  • Recent research highlights the intracellular stages of Yersinia infections.

Purpose of the Study:

  • To review recent findings on the intracellular survival mechanisms of pathogenic Yersinia.
  • To discuss the role of autophagy in Yersinia pathogenesis.
  • To explore novel host-pathogen interactions in enteric yersiniosis and plague.

Main Methods:

  • Literature review of recent studies on Yersinia-host interactions.
  • Analysis of evidence regarding Yersinia's manipulation of cellular processes.
  • Synthesis of current understanding of intracellular bacterial replication.

Main Results:

  • Pathogenic Yersinia activate autophagy in phagocytic and epithelial cells.
  • Bacteria subvert autophagosome formation to establish intracellular replication niches.
  • Autophagy plays a critical role in supporting Yersinia's intracellular survival and replication.

Conclusions:

  • Understanding Yersinia's subversion of autophagy opens new avenues for therapeutic strategies.
  • Intimate host-pathogen interactions involving autophagy are key to Yersinia pathogenesis.
  • Further research into Yersinia's intracellular lifestyle is crucial for combating yersiniosis and plague.

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