Yersinia pseudotuberculosis adhesins regulate tissue-specific colonization and immune cell localization in a mouse

Krischan J Hudson1, Amy H Bouton

  • 1Department of Microbiology, University of Virginia Health System, Box 800734, 1300 Jefferson Park Ave., Charlottesville, VA 22908-0734, USA.

Infection and Immunity
|August 22, 2006
PubMed

Insights

Yersinia pseudotuberculosis adhesin expression affects bacterial spread in mice. Invasin limits spread to the liver and spleen, while YadA promotes lung growth, impacting infection dynamics.

Area of Science:

  • Microbiology
  • Immunology
  • Infectious Diseases

Background:

  • Yersinia pseudotuberculosis utilizes adhesins like invasin and YadA for host-pathogen interactions.
  • Understanding adhesin roles is crucial for deciphering bacterial pathogenesis and immune evasion strategies.

Purpose of the Study:

  • To investigate the distinct roles of invasin and YadA adhesins in Yersinia pseudotuberculosis dissemination and colonization within a murine model.
  • To determine how adhesin deficiency influences bacterial organ tropism and host immune cell responses.

Main Methods:

  • Intravenous injection of Yersinia pseudotuberculosis mutants lacking invasin and/or YadA into BALB/c mice.
  • Assessment of bacterial colonization in liver, spleen, and lung tissues.
  • Histopathological analysis of infected tissues, focusing on leukocyte infiltration in microabscesses.

Main Results:

  • Invasin expression significantly inhibited Yersinia pseudotuberculosis colonization of the liver and spleen.
  • YadA expression decreased liver colonization but was associated with increased bacterial growth in the lungs.
  • Persistence of leukocytes within liver microabscesses correlated with enhanced bacterial colonization and reduced adhesin expression.

Conclusions:

  • Invasin and YadA exhibit differential roles in Yersinia pseudotuberculosis dissemination, influencing organ-specific colonization.
  • Adhesin expression impacts bacterial survival and growth in distinct host tissues.
  • Leukocyte persistence in microabscesses suggests a complex interplay between bacterial adhesins and the host immune response during infection.

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