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Brenda G. Byrne
Researcher at University of Michigan
Publications - 17
Citations - 1293
Brenda G. Byrne is an academic researcher from University of Michigan. The author has contributed to research in topics: Legionella pneumophila & Macrophage. The author has an hindex of 10, co-authored 17 publications receiving 1190 citations.
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Journal ArticleDOI
Cytosolic recognition of flagellin by mouse macrophages restricts Legionella pneumophila infection
Ari B. Molofsky,Brenda G. Byrne,Natalie N. Whitfield,Cressida A. Madigan,Etsu T. Fuse,Kazuhiro Tateda,Michele S. Swanson +6 more
TL;DR: In this paper, the authors reported that mouse macrophages restricted Legionella pneumophila replication and initiated a proinfl ammatory program of cell death when fl agellin contaminated their cytosol.
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Expression of Legionella pneumophila Virulence Traits in Response to Growth Conditions
TL;DR: Together, these data indicate that while nutrients are plentiful, intracellular L. pneumophila organisms are dedicated to replication; when amino acids become limiting, the progeny express virulence factors to escape the spent host, to disperse and survive in the aquatic environment, and to reestablish a protected intrACEllular niche favorable for growth.
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Inflammasome Components Coordinate Autophagy and Pyroptosis as Macrophage Responses to Infection
TL;DR: It is demonstrated for the first time that, when confronted with cytosolic contamination, primary mouse macrophages rely not only on the NLR proteins NAIP5 and NLRC4 but also on (pro-)caspase-1 protein to mount a rapid autophagic response that wards off proinflammatory cell death.
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Macrophages rapidly transfer pathogens from lipid raft vacuoles to autophagosomes.
TL;DR: A model in which macrophages exploit autophagy to capture pathogens within the lipid raft pathway for antigen presentation prior to disposal in lysosomes is discussed.
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Legionella pneumophila catalase-peroxidases are required for proper trafficking and growth in primary macrophages.
TL;DR: Quantitative similarity of the katA/B phenotypes indicates that each contributes to virulence traits largely independently of intracellular compartmentalization, supporting a model in which KatA and KatB maintain a critically low level of H2O2 compatible with proper phagosome trafficking mediated by the type IV secretion apparatus.