Invasive and adherent bacterial pathogens co-opt host clathrin for infection
2007
Veiga, Esteban | Guttman, Julian A. | Bonazzi, Matteo | Boucrot, Emmanuel | Toledo-Arana, Alejandro | Lin, Ann E. | Enninga, Jost | Pizarro-Cerda, Javier | Finlay, Brett B. | Kirchhausen, Tomas | Cossart, Pascale | Interactions Bactéries-Cellules (UIBC) ; Institut National de la Recherche Agronomique (INRA)-Institut Pasteur [Paris] (IP)-Institut National de la Santé et de la Recherche Médicale (INSERM) | Unite 604 ; Institut Naltional de la Santé et de la Recherche Médicale | Michael Smith Laboratories ; University of British Columbia [Canada] (UBC) | Harvard Medical School [Boston] (HMS) | Pathogénie Microbienne Moléculaire ; Institut Pasteur [Paris] (IP)-Institut National de la Santé et de la Recherche Médicale (INSERM) | Institut National de la Santé et de la Recherche Médicale (INSERM)
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Show more [+] Less [-]English. Infection by the bacterium Listeria monocytogenes depends on host cell clathrin. To determine whether this requirement is widespread, we analyzed infection models using diverse bacteria. We demonstrated that bacteria that enter cells following binding to cellular receptors (termed ‘‘zippering’’ bacteria) invade in a clathrin-dependent manner. In contrast, bacteria that inject effector proteins into host cells in order to gain entry (termed ‘‘triggering’’ bacteria) invade in a clathrin-independent manner. Strikingly, enteropathogenic Escherichia coli (EPEC) required clathrin to form actin-rich pedestals in host cells beneath adhering bacteria, even though this pathogen remains extracellular. Furthermore, clathrin accumulation preceded the actin rearrangements necessary for Listeria entry. These data provide evidence for a clathrin-based entry pathway allowing internalization of large objects (bacteria and ligand-coated beads) and used by ‘‘zippering’’ bacteria as part of a general mechanism to invade host mammalian cells. We also revealed a nonendocytic role for clathrin required for extracellular EPEC infections.
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