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Updated: Nov 26, 2025

Analysis of Yersinia enterocolitica Effector Translocation into Host Cells Using Beta-lactamase Effector Fusions
Published on: October 13, 2015
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.
Abstract:
Yersinia pseudotuberculosis, Y. enterocolitica and Y. pestis are pathogenic bacteria capable of causing disease in humans by growing extracellularly in lymph nodes and during systemic infections. While the capacity of these bacteria to invade, replicate, and survive within host cells has been known for long, it is only in recent years that their intracellular stages have been explored in more detail. Current evidence suggests that pathogenic Yersinia are capable of activating autophagy in both phagocytic and epithelial cells, subverting autophagosome formation to create a niche supporting bacterial intracellular replication. In this review, we discuss recent results opening novel perspectives to the understanding of intimate host-pathogens interactions taking place during enteric yersiniosis and plague.
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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