The Vibrio parahaemolyticus Type III Secretion Systems manipulate host cell MAPK for critical steps in pathogenesis

Ksenia Matlawska-Wasowska1, Rebecca Finn, Ana Mustel

  • 1Discipline of Microbiology, School of Natural Sciences, National University of Ireland, Galway, University Road, Galway, Ireland.

BMC Microbiology
|January 4, 2011
PubMed
Abstract

Insights

Vibrio parahaemolyticus uses its Type III Secretion System 1 (TTSS1) to activate MAPK pathways, leading to host cell death and IL-8 secretion. TTSS1 effector VP1680 and MAPK activation are crucial for these pathogenic effects.

Area of Science:

  • Microbiology
  • Cell Biology
  • Immunology

Background:

  • Vibrio parahaemolyticus is a foodborne pathogen that causes gastrointestinal inflammation.
  • Pathogenic strains utilize Type III Secretion Systems (TTSS) to deliver effector proteins into host cells.
  • Understanding host cell responses, particularly Mitogen Activated Protein Kinase (MAPK) activation, is crucial for V. parahaemolyticus pathogenesis.

Purpose of the Study:

  • To investigate the modulation of MAPK activation in epithelial cells by V. parahaemolyticus.
  • To determine the role of MAPK activation in bacterial cytotoxicity and Interleukin-8 (IL-8) secretion.
  • To elucidate the specific TTSS effectors involved in these host cell responses.

Main Methods:

  • Utilized Caco-2 epithelial cells and a V. parahaemolyticus O3:K6 clinical isolate (RIMD2210633).
  • Investigated MAPK (JNK, p38, ERK) activation in response to bacterial infection.
  • Identified TTSS effector proteins responsible for MAPK modulation and assessed their role in host cell death and IL-8 production.

Main Results:

  • V. parahaemolyticus TTSS1 induced JNK, p38, and ERK MAPK activation.
  • TTSS1 effector VP1680 was identified as a key mediator of MAPK activation and host cell death.
  • TTSS1 promoted IL-8 secretion, while TTSS2 inhibited IL-8 mRNA transcription early in infection.
  • VP1680 and ERK signaling were essential for V. parahaemolyticus-induced IL-8 production.

Conclusions:

  • V. parahaemolyticus activates MAPK signaling via TTSS1 and effector VP1680, contributing to pathogenesis.
  • VP1680 and MAPK activation (JNK, ERK) are critical for V. parahaemolyticus cytotoxicity.
  • Bacterial induction of IL-8 secretion is a complex process involving a balance between TTSS1 and TTSS2 activities.
  • MAPK signaling plays a significant role in the host-pathogen interactions during V. parahaemolyticus infection.

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