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.
Highlights
The genus Yersinia includes several pathogenic bacterial species for humans, which include the food-borne enteropathogens Y. enterocolitica and Y. pseudotuberculosis [1], and the vector-borne pathogen Y. pestis, the etiologic agent of plague [2]
Y. enterocolitica, Y. pseudotuberculosis, and Y. pestis produce potent effectors (Yops) that block internalization within host cells [9,10], and these microorganisms have been traditionally considered as mainly extracellular pathogens
Concerning interaction with phagocytic cells, factors required for intracellular survival of Y. pseudotuberculosis in macrophages have been shown to be required for bacterial virulence in vivo [16]
Summary
The genus Yersinia includes several pathogenic bacterial species for humans, which include the food-borne enteropathogens Y. enterocolitica and Y. pseudotuberculosis [1], and the vector-borne pathogen Y. pestis, the etiologic agent of plague [2]. During Y. enterocolitica and Y. pseudotuberculosis host infection, interaction between the bacterial surface molecule invasin and host β1-integrins promotes bacterial internalization into intestinal tract cells and colonization of Peyer’s patches and the cecum [3,4,5]. Traversal of the intestinal barrier leads to bacterial draining by local mesenteric lymph nodes, where bacterial extracellular proliferation takes place [6]. Invasin is inactivated in Y. pestis [7] and inoculation through flea bites favors pathogen draining by inguinal, axillary or cervical lymph nodes, where bacterial proliferation takes place extracellularly [8]. We summarize and discuss relevant articles describing how pathogenic Yersinia interfere with membrane trafficking and favor bacterial replication during intracellular infection stages by activating autophagy
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