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Inhibition of WAVE Regulatory Complex Activation by a Bacterial Virulence Effector Counteracts Pathogen Phagocytosis

Daniel Humphreys1, Vikash Singh1, Vassilis Koronakis1

  • 1Department of Pathology, University of Cambridge, Tennis Court Road, Cambridge CB2 1QP, UK.

Cell Reports
|October 13, 2016
PubMed

Insights

Bacteria like EPEC and EHEC evade immune cells by injecting EspG, which disrupts actin remodeling. This bacterial effector blocks host cell machinery, preventing phagocytosis and enabling extracellular survival.

Area of Science:

  • Microbiology
  • Cell Biology
  • Immunology

Background:

  • Pathogenic bacteria must evade host immune defenses, particularly phagocytosis, which is mediated by the host cell's actin cytoskeleton.
  • Macrophages utilize the WAVE regulatory complex (WRC), Arf, Rac1, and ARNO to drive actin polymerization for pathogen engulfment.

Purpose of the Study:

  • To investigate the mechanism by which enteropathogenic (EPEC) and enterohaemorrhagic (EHEC) Escherichia coli evade phagocytosis.
  • To elucidate the role of the virulence effector EspG in counteracting host cell actin remodeling and phagocytosis.

Main Methods:

  • Reconstitution of membrane-associated actin polymerization.
  • Analysis of bacterial effector protein interactions with host cell signaling molecules (Arf GTPases, ARNO).
  • Investigating the functional impact of EspG on WRC activation and actin polymerization.

Main Results:

  • The bacterial effector EspG inhibits WRC-dependent phagocytosis, allowing EPEC and EHEC to remain extracellular.
  • EspG disrupts WRC activation through dual mechanisms: interfering with Arf6-ARNO signaling and impeding Arf1-Rac1 collaboration.
  • Specific sites on Arf1 crucial for WRC activation were identified.

Conclusions:

  • EspG is a key virulence factor enabling bacterial evasion of innate immune defenses by subverting host actin dynamics.
  • Understanding EspG's mechanism provides insights into bacterial pathogenicity and host-pathogen interactions.
  • Targeting these bacterial evasion strategies could offer new therapeutic avenues.
Keywords:
ADP-ribosylation factorRho GTPaseSCAR complextype 3 secretion systemvirulence effector

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