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Javier Pizarro-Cerdá

Researcher at Pasteur Institute

Publications -  34
Citations -  4584

Javier Pizarro-Cerdá is an academic researcher from Pasteur Institute. The author has contributed to research in topics: Medicine & Biology. The author has an hindex of 19, co-authored 22 publications receiving 4282 citations. Previous affiliations of Javier Pizarro-Cerdá include French Institute of Health and Medical Research & University of Navarra.

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Journal ArticleDOI

Bacterial Adhesion and Entry into Host Cells

TL;DR: Bacteria use monomeric adhesins/invasins or highly sophisticated macromolecular machines to establish a complex host/pathogen molecular crosstalk that leads to subversion of cellular functions and establishment of disease.
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Brucella evades macrophage killing via VirB-dependent sustained interactions with the endoplasmic reticulum.

TL;DR: It is shown in a model of Brucella abortus infection of murine bone marrow–derived macrophages that a fraction of the bacteria that survive an initial macrophage killing proceed to replicate in a compartment segregated from the endocytic pathway.
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Brucella abortus transits through the autophagic pathway and replicates in the endoplasmic reticulum of nonprofessional phagocytes

TL;DR: The results are compatible with the hypothesis that pathogenic B. abortus exploits the autophagic machinery of HeLa cells to establish an intracellular niche favorable for its replication within the ER.
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A two‐component regulatory system playing a critical role in plant pathogens and endosymbionts is present in Brucella abortus and controls cell invasion and virulence

TL;DR: Two mutants showing increased sensitivity to polycations and surfactants obtained by transposon mutagenesis of virulent Brucella abortus showed that these systems have a common ancestor that has evolved to sense stimuli in plant and animal microbial environments.
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Invasion of mammalian cells by Listeria monocytogenes: functional mimicry to subvert cellular functions.

TL;DR: The bacterium Listeria monocytogenes has the unusual capacity to enter and to multiply in nonphagocytic cells as discussed by the authors, which is triggered by the two surface proteins internalin (also called InlA) and InlB, which interact with host cell receptors and either mimic or act in place of the normal cellular ligands.