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Listeriolysin O-dependent host surfaceome remodeling modulates Listeria monocytogenes invasion.


ABSTRACT: Listeria monocytogenes is a pathogenic bacterium that invades epithelial cells by activating host signaling cascades, which promote bacterial engulfment within a phagosome. The pore-forming toxin listeriolysin O (LLO), which is required for bacteria phagosomal escape, has also been associated with the activation of several signaling pathways when secreted by extracellular bacteria, including Ca2+ influx and promotion of L. monocytogenes entry. Quantitative host surfaceome analysis revealed significant quantitative remodeling of a defined set of cell surface glycoproteins upon LLO treatment, including a subset previously identified to play a role in the L. monocytogenes infection process. Our data further shows that the lysosomal-associated membrane proteins LAMP-1 and LAMP-2 are translocated to the cellular surface and those LLO-induced Ca2+ fluxes are required to trigger the surface relocalization of LAMP-1. Finally, we identify late endosomes/lysosomes as the major donor compartments of LAMP-1 upon LLO treatment and by perturbing their function, we suggest that these organelles participate in L. monocytogenes invasion.

SUBMITTER: Kuhbacher A 

PROVIDER: S-EPMC6282100 | biostudies-literature | 2018 Nov

REPOSITORIES: biostudies-literature

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Listeriolysin O-dependent host surfaceome remodeling modulates Listeria monocytogenes invasion.

Kühbacher Andreas A   Novy Karel K   Quereda Juan J JJ   Sachse Martin M   Moya-Nilges Maryse M   Wollscheid Bernd B   Cossart Pascale P   Pizarro-Cerdá Javier J  

Pathogens and disease 20181101 8


Listeria monocytogenes is a pathogenic bacterium that invades epithelial cells by activating host signaling cascades, which promote bacterial engulfment within a phagosome. The pore-forming toxin listeriolysin O (LLO), which is required for bacteria phagosomal escape, has also been associated with the activation of several signaling pathways when secreted by extracellular bacteria, including Ca2+ influx and promotion of L. monocytogenes entry. Quantitative host surfaceome analysis revealed signi  ...[more]

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