Exploitation of the host exocyst complex by bacterial pathogens

Intracellular bacterial pathogens remodel the plasma membrane of eukaryotic cells in order to establish infection. A common and well-studied mechanism of plasma membrane remodelling involves bacterial stimulation of polymerization of the host actin cytoskeleton. Here, we discuss recent results showing that several bacterial pathogens also exploit the host vesicular trafficking pathway of 'polarized exocytosis' to expand and reshape specific regions in the plasma membrane during infection. Polarized exocytosis is mediated by an evolutionarily conserved octameric protein complex termed the exocyst. We describe examples in which the bacteria Listeria monocytogenes, Salmonella enterica serovar Typhimurium, and Shigella flexneri co-opt the exocyst to promote internalization into human cells or intercellular spread within host tissues. We also discuss results showing that Legionella pneumophila or S. flexneri manipulate exocyst components to modify membrane vacuoles to favour intracellular replication or motility of bacteria. Finally, we propose potential ways that pathogens manipulate exocyst function, discuss how polarized exocytosis might promote infection and highlight the importance of future studies to determine how actin polymerization and polarized exocytosis are coordinated to achieve optimal bacterial infection.

Automated summary

Intracellular bacterial pathogens remodel the plasma membrane of eukaryotic cells to establish infection by manipulating actin cytoskeleton and polarized exocytosis. Several bacterial pathogens exploit the host vesicular trafficking pathway of polarized exocytosis, mediated by the exocyst protein complex, to expand and reshape specific regions in the plasma membrane. They also manipulate exocyst components to promote internalization or intercellular spread within host tissues, modify membrane vacuoles, and favor intracellular replication or motility. Coordinating actin polymerization and polarized exocytosis is crucial for optimal bacterial infection.