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Yersinia enterocolitica, a primary model for bacterial invasiveness
Reviews of Infectious Diseases
|January 1, 1987
Summary
Yersinia enterocolitica, a frequent cause of infection, exhibits varying virulence. Its calcium (Ca++) dependence and virulence are linked to a plasmid, making it a model for bacterial invasiveness research.
Area of Science:
- Microbiology
- Bacterial Pathogenesis
- Molecular Biology
Background:
- Yersinia enterocolitica is a significant pathogen in human and animal infections, with American strains showing higher virulence.
- A link between Y. enterocolitica and Yersinia pestis was established through the discovery of Ca++ dependence at 37°C.
- This Ca++ requirement is plasmid-dependent and crucial for virulence, leading to Y. enterocolitica's use as a model for bacterial invasiveness.
Purpose of the Study:
- To investigate the factors contributing to Yersinia enterocolitica's virulence and Ca++ dependence.
- To understand the role of plasmid-encoded genes in bacterial invasiveness.
- To explore the genetic basis of Y. enterocolitica's interaction with host cells.
Main Methods:
- Comparative analysis of virulent and non-virulent Y. enterocolitica strains.
- Plasmid analysis to identify genes responsible for Ca++ dependence and virulence.
- Investigating bacterial growth under varying Ca++ concentrations.
- Studying the role of chromosomal genes in host cell interaction.
Main Results:
- Virulence and Ca++ dependence in Y. enterocolitica are linked to a 70-kilobase plasmid.
- Plasmid-encoded outer membrane proteins are synthesized during the immune response phase.
- Mutants affecting Ca++ dependence also exhibit altered growth at 37°C.
- Evidence suggests chromosomal genes, not the pYV plasmid, are involved in intestinal epithelial cell endocytosis.
Conclusions:
- The 70-kilobase plasmid plays a critical role in Y. enterocolitica virulence and Ca++ dependence.
- Understanding Ca++ dependence provides insights into bacterial adaptation and immune system evasion.
- Chromosomal factors are essential for the initial steps of Yersinia infection, particularly host cell entry.