Interaction of microbial pathogens with host exocytic pathways

Cell Microbiol. 2018 Aug;20(8):e12861. doi: 10.1111/cmi.12861. Epub 2018 Jun 20.

Abstract

Many microbial pathogens co-opt or perturb host membrane trafficking pathways. This review covers recent examples in which microbes interact with host exocytosis, the fusion of intracellular vesicles with the plasma membrane. The bacterial pathogens Listeria monocytogenes and Staphylococcus aureus subvert recycling endosomal pathways of exocytosis in order to induce their entry into human cells. By contrast, entry of the protozoan pathogen Trypanosoma cruzi or the virus adenovirus into host cells involves exploitation of lysosomal exocytosis. Toxins produced by Bacillus anthracis or Vibrio cholerae interfere with exocytosis pathways mediated by the GTPase Rab11 and the exocyst complex. By doing so, anthrax or cholera toxins impair recycling of cadherins to cell-cell junctions and disrupt the barrier properties of endothelial cells or intestinal epithelial cells, respectively. Uropathogenic Escherichia coli (UPEC) is expelled from bladder epithelial cells through two different exocytic routes that involve sensing of bacteria in vacuoles by host Toll-like receptor 4 (TLR4) or monitoring of the pH of lysosomes harbouring UPEC. The TLR4 pathway is mediated by multiple Rab GTPases and the exocyst, whereas the other pathway involves exocytosis of lysosomes. Expulsion of UPEC through these pathways is thought to benefit the host.

Keywords: cell injury/sub-lethal injury; cell membrane; infection; interaction; microbial-cell; toxins; virulence.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Bacteria / pathogenicity*
  • Cell Membrane / metabolism*
  • Cytoplasmic Vesicles / metabolism*
  • Cytoplasmic Vesicles / microbiology
  • Exocytosis*
  • Host-Pathogen Interactions*
  • Humans
  • Trypanosoma / pathogenicity*
  • Viruses / pathogenicity*