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  • Review Article
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RAB11-mediated trafficking in host–pathogen interactions

Nature Reviews Microbiology volume 12, pages 624–634 (2014)Cite this article

Subjects

Key Points

  • Bacterial and viral pathogens disrupt or exploit RAB11 and exocyst-dependent vesicular trafficking.

  • Innate immune signalling, autophagy and toxin shedding are regulated by RAB11 and the exocyst.

  • Toxins that increase intracellular cyclic AMP levels inhibit endocytic recycling of proteins to cell junctions, thereby disrupting vascular endothelial and epithelial barrier integrity.

  • Bacterial pathogens exploit endocytic recycling to divert host resources to sites of bacterial invasion.

  • Disruption of trafficking from the Golgi complex to recycling endosomes contributes to pathogen replication.

  • Viruses subvert endocytic recycling to exit from host cells.

Abstract

Many bacterial and viral pathogens block or subvert host cellular processes to promote successful infection. One host protein that is targeted by invading pathogens is the small GTPase RAB11, which functions in vesicular trafficking. RAB11 functions in conjunction with a protein complex known as the exocyst to mediate terminal steps in cargo transport via the recycling endosome to cell–cell junctions, phagosomes and cellular protrusions. These processes contribute to host innate immunity by promoting epithelial and endothelial barrier integrity, sensing and immobilizing pathogens and repairing pathogen-induced cellular damage. In this Review, we discuss the various mechanisms that pathogens have evolved to disrupt or subvert RAB11-dependent pathways as part of their infection strategy.

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Figure 1: RAB-mediated endocytic recycling.
Figure 2: The modes of action of anthrax toxins and cholera toxin.
Figure 3: Pathogen subversion of RAB11 and exocyst functions.
Figure 4: Viral exit via the recycling endosome.

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Acknowledgements

The authors thank E. Troemel and members of the Bier and Nizet laboratories for helpful comments and discussions on the manuscript. They also acknowledge funding from the following US National Institutes of Health (NIH) R01 grants: AI070654 (to E.B.), AI057153 (to V.N.) and AI110713 (to E.B. and V.N.), which have supported their studies on topics covered in this Review.

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Authors and Affiliations

  1. Section of Cell and Developmental Biology, University of California, San Diego, 9500 Gilman Drive, La Jolla, 92093, California, USA

    Annabel Guichard & Ethan Bier

  2. Department of Pediatrics, University of California, San Diego, 9500 Gilman Drive, La Jolla, 92093, California, USA

    Victor Nizet

  3. Skaggs School of Pharmacy and Pharmaceutical Sciences, University of California, San Diego, 9500 Gilman Drive, La Jolla, 92093, California, USA

    Victor Nizet

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Correspondence to Victor Nizet or Ethan Bier.

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PowerPoint slides

Glossary

Recycling endosomes

Late vesicular compartments that are involved in recycling membrane proteins and de novo synthesized cargo from the Golgi complex to the cell surface.

SNARE complexes

(Soluble NSF attachment protein receptor complexes). A family of related proteins that mediate the fusion of surface-bound vesicles with the plasma membrane (for example, SNAP25, a plasma membrane tethered SNARE and a vesicular SNARE form a trimeric complex to initiate membrane fusion).

Invadosomes

Subcellular structures that derive from the plasma membrane and mediate bacterial invasion of the host cell.

Notch signalling

A signalling pathway that controls a range of cell fate and growth decisions. It is activated at adherens junctions by cell surface-tethered ligands (for example, Delta) on one cell, which stimulate Notch receptors on adjacent cells.

Adherens junctions

Subapically localized cell–cell junctions that consist of transmembrane epithelial cadherin adhesion molecules, which interact with the cytoskeleton via α-catenins and β-catenins and link epithelial and endothelial cells, enabling them to form contiguous sheets.

Tight junctions

The most apically localized cell–cell junctions; they consist of adhesive claudins and occludin transmembrane proteins, which function as a diffusion barrier to ions, water and other small molecules.

Toxisome

A vesicle that contains toxic factors and that is expelled from the cell surface (for example, shed microvilli).

Anterograde Golgi trafficking

A pathway via which vesicles that are derived from Golgi membranes are directed to the cell surface via anterograde trafficking. In addition, vesicles that are derived from the cell surface or other intracellular membrane compartments can be directed back to the Golgi via retrograde trafficking.

RALB

A small GTPase that can bind in a mutually exclusive manner to either of the exocyst components SEC5 or EXO84 to function as a molecular switch between immune signalling and autophagy.

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Guichard, A., Nizet, V. & Bier, E. RAB11-mediated trafficking in host–pathogen interactions. Nat Rev Microbiol 12, 624–634 (2014). https://doi.org/10.1038/nrmicro3325

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