Host-pathogen interactions: the seduction of molecular cross talk - PubMed (original) (raw)

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Host-pathogen interactions: the seduction of molecular cross talk

P Sansonetti. Gut. 2002 May.

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.

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Figures

Figure 1

Figure 1

A paradigm of "zippering" entry of a bacterial pathogen into epithelial cells. Invasin mediated binding of Yersinia pseudotuberculosis to ß1 integrins and internalisation.

Figure 2

Figure 2

A paradigm or "triggering" entry of pathogens into epithelial cells: TTSS mediated translocation of Salmonella and Shigella effectors of entry inducing the formation of a macropinocytic vacuole.

Figure 3

Figure 3

Structure of the TTSS of Shigella flexneri. OM, outer membrane; PS, periplasmic space; IM, inner membrane; Cyt, cytoplasm.

Figure 4

Figure 4

Physiopathological scheme of Shigella infection.

Figure 5

Figure 5

Physiopathological scheme of Yersinia infection.

Figure 6

Figure 6

Salmonella routes for crossing the intestinal barrier and physiopathological scheme of infection.

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