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The enteropathogenic E. coli effector EspB facilitates microvillus effacing and antiphagocytosis by inhibiting myosin

Yosuke Iizumi1, Hiroshi Sagara, Yasuaki Kabe

  • 1Graduate School of Bioscience and Biotechnology, Tokyo Institute of Technology, 4259 Nagatsuta-cho, Midori-ku, Yokohama 226-8501, Japan.

Cell Host & Microbe
|December 15, 2007
PubMed

Insights

Enteropathogenic Escherichia coli (EPEC) uses EspB to bind and inhibit host cell myosins, crucial for intestinal functions. This EspB-myosin interaction is key for EPEC

Area of Science:

  • Microbiology
  • Cell Biology
  • Pathogen-Host Interactions

Background:

  • Enteropathogenic Escherichia coli (EPEC) utilizes a type III secretion system (TTSS) to inject effector proteins into host cells.
  • EPEC infection disrupts intestinal microvilli and inhibits phagocytosis, crucial immune processes.
  • The specific role of the TTSS effector EspB within the host cell cytoplasm is not well understood.

Purpose of the Study:

  • To elucidate the physiological functions of the EPEC TTSS effector EspB within the host cell cytoplasm.
  • To investigate the interaction between EspB and host cell proteins, particularly myosins.
  • To determine the role of EspB's myosin-binding activity in EPEC pathogenesis.

Main Methods:

  • Investigated the interaction of EspB with myosins using biochemical assays.
  • Utilized EspB mutants lacking myosin-binding regions to assess functional consequences.
  • Assessed the role of EspB's myosin-binding region in Citrobacter rodentium murine infection models.

Main Results:

  • EspB directly binds to myosins, a protein superfamily involved in actin-based cellular processes.
  • EspB inhibits the interaction between myosins and actin filaments.
  • An EspB mutant unable to bind myosins retained TTSS function but failed to induce microvillus effacement or suppress phagocytosis.
  • The myosin-binding region of EspB is essential for efficient infection by the related pathogen Citrobacter rodentium in mice.

Conclusions:

  • EspB's interaction with and inhibition of host cell myosins is a critical mechanism for EPEC pathogenesis.
  • Inhibition of myosin function by EspB contributes to EPEC's ability to destroy microvilli and evade phagocytosis.
  • Targeting the EspB-myosin interaction could represent a novel therapeutic strategy against EPEC and related infections.

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