Unique Cell Adhesion and Invasion Properties of Yersinia enterocolitica O:3, the Most Frequent Cause of Human Yersiniosis

PLoS Pathogens

Alexander Rakin¹  Jürgen Heesemann²  Mikael Skurnik³  Julia Schaake⁴  Frank Uliczka⁴  Angelika Fruth⁴  Tatjana Stolz⁴  Eckhard Strauch⁵  Manfred Rohde⁵  Fabio Pisano⁵  Petra Dersch⁶  Julia Batzilla⁷ 

[1] Bundesinstitut für Risikoforschung, Berlin, Germany;Department of Bacteriology and Immunology, The Haartman Institute, University of Helsinki and Helsinki University Central Hospital Laboratory Diagnostics, Helsinki, Finland;Department of Medical Microbiology, Helmholtz-Zentrum für Infektionsforschung, Braunschweig, Germany;Department of Molecular Infection Biology, Helmholtz-Zentrum für Infektionsforschung, Braunschweig, Germany;Institut für Mikrobiologie, Technische Universität Braunschweig, Braunschweig, Germany;Max von Pettenkofer Institut, Ludwigs-Maximilians-Universität, München, Germany;Robert Koch-Institut, Wernigerode, Germany

关键词: Yersinia enterocolitica;    Host cells;    Virulence factors;    Gene expression;    Pathogen motility;    Plasmid construction;    Yersinia pseudotuberculosis;    Body temperature;   

DOI  :  10.1371/journal.ppat.1002117

学科分类：生物科学（综合）

来源: Public Library of Science

【 摘 要 】

Many enteric pathogens are equipped with multiple cell adhesion factors which are important for host tissue colonization and virulence. Y. enterocolitica, a common food-borne pathogen with invasive properties, uses the surface proteins invasin and YadA for host cell binding and entry. In this study, we demonstrate unique cell adhesion and invasion properties of Y. enterocolitica serotype O:3 strains, the most frequent cause of human yersiniosis, and show that these differences are mainly attributable to variations affecting the function and expression of invasin in response to temperature. In contrast to other enteric Yersinia strains, invasin production in O:3 strains is constitutive and largely enhanced compared to other Y. enterocolitica serotypes, in which invA expression is temperature-regulated and significantly reduced at 37°C. Increase of invasin levels is caused by (i) an IS1667 insertion into the invA promoter region, which includes an additional promoter and RovA and H-NS binding sites, and (ii) a P98S substitution in the invA activator protein RovA rendering the regulator less susceptible to proteolysis. Both variations were shown to influence bacterial colonization in a murine infection model. Furthermore, we found that co-expression of YadA and down-regulation of the O-antigen at 37°C is required to allow efficient internalization by the InvA protein. We conclude that even small variations in the expression of virulence factors can provoke a major difference in the virulence properties of closely related pathogens which may confer better survival or a higher pathogenic potential in a certain host or host environment.

【 授权许可】

CC BY