Targeting membrane trafficking in infection prophylaxis: dynamin inhibitors

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Callista B Harper1, Michel R Popoff, Adam McCluskey

  • 1Queensland Brain Institute, University of Queensland, Brisbane, Queensland 4072, Australia.

Trends in Cell Biology
|November 21, 2012
PubMed

Insights

Many pathogens use dynamin-dependent pathways to infect cells. Inhibiting dynamin offers a potential therapeutic strategy against these infections, though careful consideration of methods and pitfalls is needed.

Area of Science:

  • Cellular biology
  • Microbiology
  • Pharmacology

Background:

  • Pathogens frequently exploit host cell endocytic pathways for entry and toxicity.
  • Dynamin, a GTPase, plays a crucial role in various stages of cellular trafficking and pathogen intoxication.
  • Understanding pathogen-host interactions at the molecular level is key to developing novel therapeutics.

Purpose of the Study:

  • To review pathogens that rely on dynamin-dependent endocytosis for cellular intoxication.
  • To outline the internalization mechanisms employed by these pathogens.
  • To evaluate the therapeutic potential of targeting dynamin function.

Main Methods:

  • Literature review of pathogens utilizing dynamin-dependent trafficking.
  • Analysis of pathogen internalization mechanisms.
  • Assessment of pharmacological and genetic inhibition of dynamin.
  • Evaluation of methodologies for studying dynamin's role in intoxication.

Main Results:

  • A growing number of pathogens, including bacteria, viruses, and toxins, require dynamin-dependent trafficking for cellular entry and toxicity.
  • Pharmacological and genetic targeting of dynamin has demonstrated protective effects against pathogen intoxication.
  • Various methodologies exist to investigate dynamin's role, each with specific advantages and limitations.

Conclusions:

  • Dynamin-dependent endocytosis is a common mechanism exploited by diverse pathogens.
  • Dynamin inhibitors (DIs) represent a promising prophylactic and therapeutic strategy against pathogen-mediated cellular damage.
  • Further research is needed to optimize the use of DIs and address potential pitfalls in their therapeutic application.

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