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1. A Role for Taok2 in Listeria monocytogenes Vacuolar Escape.

Author

Quereda, Juan J, Morel, Camille, Lopez-Montero, Noelia, Ziveri, Jason, Rolland, Steven, Grenier, Théodore, Aulner, Nathalie, Danckaert, Anne, Charbit, Alain, Enninga, Jost, Cossart, Pascale, and Pizarro-Cerdá, Javier

Subjects
*LISTERIA monocytogenes, *SMALL interfering RNA, *EPITHELIAL cells, *BACTERIAL toxins, *PROTEINS, *LISTERIA, *LISTERIOSIS, *CYTOPLASM
Abstract

The bacterial pathogen Listeria monocytogenes invades host cells, ruptures the internalization vacuole, and reaches the cytosol for replication. A high-content small interfering RNA (siRNA) microscopy screen allowed us to identify epithelial cell factors involved in L. monocytogenes vacuolar rupture, including the serine/threonine kinase Taok2. Kinase activity inhibition using a specific drug validated a role for Taok2 in favoring L. monocytogenes cytoplasmic access. Furthermore, we showed that Taok2 recruitment to L. monocytogenes vacuoles requires the presence of pore-forming toxin listeriolysin O. Overall, our study identified the first set of host factors modulating L. monocytogenes vacuolar rupture and cytoplasmic access in epithelial cells. [ABSTRACT FROM AUTHOR]

Published
2022
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2. A Role for Taok2 in Listeria monocytogenes Vacuolar Escape

Author

Alain Charbit, Jost Enninga, Nathalie Aulner, Noelia Lopez-Montero, Jason Ziveri, Steven Rolland, Javier Pizarro-Cerdá, Pascale Cossart, Camille Morel, Juan J. Quereda, Théodore Grenier, Anne Danckaert, Interactions Bactéries-Cellules (UIBC), Institut Pasteur [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE), Universidad Cardenal Herrera-CEU (CEU-UCH), Dynamique des Interactions Hôte-Pathogène - Dynamics of Host-Pathogen Interactions, Institut Pasteur [Paris]-Centre National de la Recherche Scientifique (CNRS), Institut Necker Enfants-Malades (INEM - UM 111 (UMR 8253 / U1151)), Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université de Paris (UP), Institut de Génomique Fonctionnelle de Lyon (IGFL), École normale supérieure - Lyon (ENS Lyon)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Centre National de la Recherche Scientifique (CNRS)-Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE), Institut Pasteur [Paris], Yersinia, Institut National de la Recherche Agronomique (INRA)-Institut Pasteur [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM), Université Paris Descartes, Sorbonne Paris Cité, Paris, France, Inflammasome NLRP3 – NLRP3 Inflammasome, Centre International de Recherche en Infectiologie - UMR (CIRI), Université de Lyon-Université de Lyon-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-École normale supérieure - Lyon (ENS Lyon)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), BioImagerie Photonique – Photonic BioImaging (UTechS PBI), This work was supported by Institut Pasteur, Université Paris Diderot, Agence Nationale de la Recherche (grant numbers ANR-15-CE15-0017 StopBugEntry to J. P. C., J. E., and A. C., and ANR-10-INSB-04-01, France-BioImaging to N. A.). J. J. Q. is supported by the Spanish Ministry of Science, Innovation and Universities (grant number RYC-2018-024985-I Ramón y Cajal contract). J. E. was supported by the European Research Council (consolidator grant EndoSubvert). P. B. I. is supported by the Région Ile de France (DIM1Health) and Groupement d’Intérêt Scientifique Infrastructures en Biologie Santé et Agronomie. The teams of P. C., J. P. C., N. A., and J. E. are members of Laboratory of Excellence Integrative Biology of Emerging Infectious Diseases., ANR-15-CE15-0017,StopBugEntry,Identification des nouvelles molécules cellulaires cibles pour combattre les infections bactériennes(2015), ANR-10-INBS-0004,France-BioImaging,Développment d'une infrastructure française distribuée coordonnée(2010), ANR-10-LABX-0062,IBEID,Integrative Biology of Emerging Infectious Diseases(2010), European Project: 682809,EndoSubvert(2017), Producción Científica UCH 2022, UCH. Departamento de Producción y Sanidad Animal, Salud Pública Veterinaria y Ciencia y Tecnología de los Alimentos, Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Charbit, Alain, Identification des nouvelles molécules cellulaires cibles pour combattre les infections bactériennes - - StopBugEntry2015 - ANR-15-CE15-0017 - AAPG2015 - VALID, Développment d'une infrastructure française distribuée coordonnée - - France-BioImaging2010 - ANR-10-INBS-0004 - INBS - VALID, Integrative Biology of Emerging Infectious Diseases - - IBEID2010 - ANR-10-LABX-0062 - LABX - VALID, Common mechanisms of host membrane trafficking subversion by intracellular pathogens to rupture bacterial containing vacuoles - EndoSubvert - 2017-01-01 - 2021-12-31 - 682809 - VALID, Institut National de la Recherche Agronomique (INRA)-Institut Pasteur [Paris] (IP)-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut Pasteur [Paris] (IP)-Centre National de la Recherche Scientifique (CNRS), Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Paris Cité (UPCité), Institut Pasteur [Paris] (IP), Centre International de Recherche en Infectiologie (CIRI), École normale supérieure de Lyon (ENS de Lyon)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Université Jean Monnet - Saint-Étienne (UJM)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-École normale supérieure de Lyon (ENS de Lyon)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Université Jean Monnet - Saint-Étienne (UJM)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), and Producción Científica UCH 2020

Subjects
0301 basic medicine, Cytoplasm, media_common.quotation_subject, Citoplasma, 030106 microbiology, Vacuole, Biology, medicine.disease_cause, Pathogenic bacteria, 03 medical and health sciences, Hemolysin Proteins, Cytosol, Listeria monocytogenes, Bacterial Proteins, [SDV.MHEP.MI]Life Sciences [q-bio]/Human health and pathology/Infectious diseases, medicine, Immunology and Allergy, Humans, Células epiteliales, vacuolar escape, Listeriosis, Kinase activity, Internalization, Pathogen, ComputingMilieux_MISCELLANEOUS, media_common, Epithelial cells, siRNA screen, Kinase, [SDV.MP.BAC]Life Sciences [q-bio]/Microbiology and Parasitology/Bacteriology, Cell biology, STE1-like kinase, 030104 developmental biology, Infectious Diseases, [SDV.MP]Life Sciences [q-bio]/Microbiology and Parasitology, Bacterias patógenas, Vacuoles, [SDV.MHEP.MI] Life Sciences [q-bio]/Human health and pathology/Infectious diseases, [SDV.MP.BAC] Life Sciences [q-bio]/Microbiology and Parasitology/Bacteriology, Taok2
Abstract

Este artículo se encuentra disponible en la siguiente URL: https://academic.oup.com/jid/advance-article/doi/10.1093/infdis/jiaa367/5862450 En esta investigación también participan: Nathalie Aulner, Anne Danckaert, Alain Charbit, Jost Enninga, Pascale Cossart y Javier Pizarro Cerdá. The bacterial pathogen Listeria monocytogenes invades host cells, ruptures the internalization vacuole, and reaches the cytosol for replication. A high-content small interfering RNA (siRNA) microscopy screen allowed us to identify epithelial cell factors involved in L. monocytogenes vacuolar rupture, including the serine/threonine kinase Taok2. Kinase activity inhibition using a specific drug validated a role for Taok2 in favoring L. monocytogenes cytoplasmic access. Furthermore, we showed that Taok2 recruitment to L. monocytogenes vacuoles requires the presence of pore-forming toxin listeriolysin O. Overall, our study identified the first set of host factors modulating L. monocytogenes vacuolar rupture and cytoplasmic access in epithelial cells.

Published
2021
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3. Pathways of host cell exit by intracellular pathogens

Author

Georg Häcker, Antje Flieger, Freddy Frischknecht, Mathias W. Hornef, and Gabriele Pradel

Subjects
0301 basic medicine, Programmed cell death, membrane lysis, Lysis, host cell, Review, Biochemistry, Genetics and Molecular Biology (miscellaneous), Microbiology, Applied Microbiology and Biotechnology, 03 medical and health sciences, Virology, ddc:570, Genetics, vacuolar escape, ddc:610, Molecular Biology, Pathogen, lcsh:QH301-705.5, programmed cell death, biology, Host (biology), Intracellular parasite, exit, compartment, Cell Biology, biology.organism_classification, Cell biology, egress, 030104 developmental biology, lcsh:Biology (General), Protozoa, Parasitology, 610 Medizin und Gesundheit, Bacteria, Intracellular, pathogen
Abstract

Microbial cell 5(12), 525-544 (2018). doi:10.15698/mic2018.12.659, Published by Shared Science Publ., Graz

Published
2018
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4. Vacuolar escape of foodborne bacterial pathogens.

Author

Bianchi, Frans and van den Bogaart, Geert

Subjects
*FOOD pathogens, *SALMONELLA enterica, *FOODBORNE diseases, *INTRACELLULAR pathogens, *LISTERIA monocytogenes, *FOOD contamination, *EPITHELIAL cells
Abstract

The intracellular pathogens Listeria monocytogenes, Salmonella enterica, Shigella spp. and Staphylococcus aureus are major causes of foodborne illnesses. Following the ingestion of contaminated food or beverages, pathogens can invade epithelial cells, immune cells and other cell types. Pathogens survive and proliferate intracellularly via two main strategies. First, the pathogens can remain in membrane-bound vacuoles and tailor organellar trafficking to evade host-cell defenses and gain access to nutrients. Second, pathogens can rupture the vacuolar membrane and proliferate within the nutrient-rich cytosol of the host cell. Although this virulence strategy of vacuolar escape is well known for L. monocytogenes and Shigella spp., it has recently become clear that S. aureus and Salmonella spp. also gain access to the cytosol, and that this is important for their survival and growth. In this Review, we discuss the molecular mechanisms of how these intracellular pathogens rupture the vacuolar membrane by secreting a combination of proteins that lyse the membranes or that remodel the lipids of the vacuolar membrane, such as phospholipases. In addition, we also propose that oxidation of the vacuolar membrane also contributes to cytosolic pathogen escape. Understanding these escape mechanisms could aid in the identification of new therapeutic approaches to combat foodborne pathogens. [ABSTRACT FROM AUTHOR]

Published
2021
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