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A rationale for repression and/or loss of motility by pathogenic Yersinia in the mammalian host

Scott A Minnich1, Harold N Rohde

  • 1Department of Microbiology, Molecular Biology, and Biochemistry, University of Idaho, Moscow, USA. sminnich@uidaho.edu

Advances in Experimental Medicine and Biology
|October 31, 2007
PubMed

Insights

Pathogenic Yersinia bacteria repress flagella, or motility structures, in hosts. This prevents immune detection and maintains virulence, suggesting motility is detrimental for these bacteria in mammals.

Area of Science:

  • Microbiology
  • Bacterial Pathogenesis
  • Molecular Biology

Background:

  • Pathogenic Yersinia species exhibit varied regulation of flagellar motility.
  • Flagella and their components, like flagellins, can be recognized by host immune systems.
  • Motility can be a disadvantage for bacterial pathogens within a mammalian host.

Purpose of the Study:

  • To investigate the mechanisms and implications of flagellar repression in pathogenic Yersinia.
  • To understand why Yersinia species suppress flagellar synthesis during host infection.

Main Methods:

  • Comparative analysis of flagellar gene expression in different Yersinia species.
  • Examination of regulatory pathways, including fliA (sigmaF) and flhD.
  • Assessment of virulence in Yersinia enterocolitica with artificially expressed flagellin.

Main Results:

  • Enteropathogenic Yersinia (Y. enterocolitica, Y. pseudotuberculosis) repress flagella synthesis via fliA (sigmaF) repression.
  • Yersinia pestis has mutations in flagellar genes, including flhD, leading to loss of flagellar capability.
  • Repression of flagellins prevents their recognition by type III secretion systems and reduces innate immune stimulation.
  • Artificial flagellin expression in Y. enterocolitica significantly reduces virulence.

Conclusions:

  • Flagellar repression is a key strategy for pathogenic Yersinia to evade host immunity and maintain virulence.
  • Motility, mediated by flagella, appears to be a liability for Yersinia in the mammalian host environment.
  • Understanding these mechanisms offers insights into bacterial adaptation and host-pathogen interactions.

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