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Host–pathogen interactions: the seduction of molecular cross talk
  1. P Sansonetti
  1. Unité de Pathogénie Microbienne Moléculaire, INSERM U389, Institut Pasteur, Paris, France
  1. Correspondence to:
    Dr P Sansonetti, Unité de Pathogénie Microbienne Moléculaire, INSERM U389, Institut Pasteur, 28 Rue du Docteur Roux, 75724, Paris cedex 15, France;
    psanson{at}pasteur.fr

Abstract

Bacterial pathogens have evolved two major strategies to colonise the intestinal epithelium. Adherent microorganisms bind to the apical pole of the intestinal epithelium, whereas invasive microorganisms disrupt and invade the epithelium. Recognition of the genetic bases of bacterial pathogenicity and analysis of the molecular cross talks established between pathogens and their mammalian target cells have illuminated this diversity of interactions. We have compared the strategies of enteroinvasive pathogens, with emphasis on bacterial species such as Shigella, Yersinia, and Salmonella, that represent paradigms of interaction. Cross talks leading to alteration of the epithelial cell actin cytoskeleton appear as a recurrent theme during entry and dissemination into epithelial cells. Other cross talks alter the trafficking of cellular vesicles and induce changes in the intracellular compartment in which they reside, thus creating niches favourable to bacterial survival and growth. Finally, a variety of strategies also exist to deal with other components of the epithelial barrier, such as macrophages. Pro-phagocytic, anti-phagocytic, and pro-apoptotic processes appear to be of particular importance.

  • host
  • pathogen
  • intestine
  • epithelium
  • bacteria
  • CT, cholera toxin
  • EHEC, enterohaemorrhagic E coli
  • EPEC, enteropathogenic E coli
  • ETEC, enterotoxigenic E coli
  • FAE, follicle associated epithelium
  • GAP, GTPase activating protein
  • GRR, glycine rich repeat
  • LT, thermolabile
  • PMN, polymorphonuclear leucocyte
  • SLT, Shiga like toxin
  • ST, thermostable
  • TTSS, type III secretory system

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