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Yersinia outer proteins: role in modulation of host cell signaling responses and pathogenesis

Gloria I Viboud1, James B Bliska

  • 1Department of Molecular Genetics and Microbiology, Center for Infectious Diseases, SUNY Stony Brook, Stony Brook, New York 11794-5222, USA. gviboud@ms.cc.sunysb.edu

Annual Review of Microbiology
|April 26, 2005
PubMed

Insights

Pathogenic Yersinia bacteria use a type III secretion system (TTSS) to inject Yersinia outer proteins (Yops) into host cells. These Yops disrupt host signaling pathways, enabling bacterial survival and virulence.

Area of Science:

  • Microbiology
  • Immunology
  • Molecular Biology

Background:

  • Pathogenic Yersinia species utilize a common virulence plasmid encoding a type III secretion system (TTSS).
  • This TTSS is essential for Yersinia survival and replication within host lymphoid tissues.
  • The TTSS exports Yersinia outer proteins (Yops), critical pathogenicity factors.

Purpose of the Study:

  • To review the biochemical functions of Yops.
  • To elucidate the signaling pathways modulated by Yops.
  • To understand the role of Yops in Yersinia pathogenesis and virulence.

Main Methods:

  • Focus on reviewing established biochemical functions of effector Yops.
  • Analysis of Yop interactions with host cell signaling pathways.
  • Examination of the impact of Yop activities on immune responses.

Main Results:

  • Two translocator Yops (YopB, YopD) mediate effector Yop translocation into host cell cytosol.
  • Six effector Yops (YopO, YopH, YopM, YopT, YopJ, YopE) counteract host signaling initiated by various receptors.
  • Yop activity effectively thwarts innate and adaptive immune responses.

Conclusions:

  • Yops are crucial virulence factors that manipulate host cell signaling to promote Yersinia infection.
  • Understanding Yop functions provides insights into bacterial pathogenesis mechanisms.
  • Targeting the TTSS or Yops could be potential strategies for controlling Yersinia infections.

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