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The biology of the cytolethal distending toxins

Lina Guerra1, Ximena Cortes-Bratti, Riccardo Guidi

  • 1Department of Cell and Molecular Biology, Karolinska Institute, Stockholm, Sweden, Box 285, S-171 77 Stockholm, Sweden. lina.guerra@ki.se

Toxins
|November 10, 2011
PubMed

Insights

Cytolethal distending toxins (CDTs) are bacterial genotoxins causing DNA damage. This review details CDT mechanisms, cellular responses, and remaining questions in toxin biology.

Area of Science:

  • Microbiology
  • Toxicology
  • Cell Biology

Background:

  • Cytolethal distending toxins (CDTs) are bacterial genotoxins produced by Gram-negative pathogens.
  • CDTs cause DNA damage in target cells, leading to cell cycle arrest and apoptosis or senescence.
  • The precise surface receptor for CDT binding remains poorly characterized.

Purpose of the Study:

  • To review the well-characterized aspects of cytolethal distending toxin (CDT) biology.
  • To discuss the mechanisms of CDT internalization, transport, and nuclear translocation.
  • To highlight unanswered questions regarding CDT-host cell interactions.

Main Methods:

  • Review of existing literature on CDT structure, function, and cellular effects.
  • Analysis of toxin internalization pathways, including lipid raft dependence and dynamin-dependent endocytosis.
  • Examination of intracellular trafficking, nuclear translocation, and DNA damage response activation.

Main Results:

  • CDT is an A-B(2) toxin with CdtA and CdtC subunits mediating cell surface binding and CdtB mediating DNA damage.
  • Toxin internalization requires intact lipid rafts and occurs via dynamin-dependent endocytosis.
  • The toxin undergoes retrograde transport through the Golgi and ER before nuclear translocation.

Conclusions:

  • CDT intoxication triggers DNA damage responses, cell cycle arrest, and DNA repair activation.
  • Cells unable to repair CDT-induced DNA damage undergo senescence or apoptosis.
  • Further research is needed to fully elucidate CDT receptor interactions and biological functions.
Keywords:
DNA damageDNA damage responsebacterial genotoxinchancroidcolitis/hepatitiscytolethal distending toxinperiodontitissurvival signalstoxin internalizationvirulence factor

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