T
Tessa Bergsbaken
Researcher at University of Washington
Publications - 21
Citations - 4001
Tessa Bergsbaken is an academic researcher from University of Washington. The author has contributed to research in topics: Pyroptosis & Caspase 1. The author has an hindex of 12, co-authored 17 publications receiving 3213 citations. Previous affiliations of Tessa Bergsbaken include University of Wisconsin-Madison.
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Journal ArticleDOI
Pyroptosis: host cell death and inflammation
TL;DR: Pyroptosis, or caspase 1-dependent cell death, is inherently inflammatory, is triggered by various pathological stimuli, such as stroke, heart attack or cancer, and is crucial for controlling microbial infections.
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Anthrax lethal toxin and Salmonella elicit the common cell death pathway of caspase-1-dependent pyroptosis via distinct mechanisms
TL;DR: It is demonstrated that distinct activation pathways elicit the conserved cell death effector mechanism of caspase-1-mediated pyroptosis and support the notion that this pathway of proinflammatory programmed cell death is broadly relevant to cell death and inflammation invoked by diverse stimuli.
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Biogenesis of bacterial membrane vesicles.
Brooke L. Deatherage,J. Cano Lara,Tessa Bergsbaken,Sara L. Rassoulian Barrett,Stephanie Lara,Brad T. Cookson +5 more
TL;DR: These data support a model of MV biogenesis, wherein bacterial growth and division invoke temporary, localized reductions in the density of OM–PG and OM-PG–IM associations within the envelope structure, thus releasing OM as MVs.
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Proinflammatory microenvironments within the intestine regulate the differentiation of tissue-resident CD8+ T cells responding to infection
TL;DR: The studies have identified the 'preferential' development of CD103− TRM cells in inflammatory microenvironments within the lamina propria and suggest that this subset has a critical role in controlling infection.
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Macrophage Activation Redirects Yersinia-Infected Host Cell Death from Apoptosis to Caspase-1-Dependent Pyroptosis
Tessa Bergsbaken,Brad T. Cookson +1 more
TL;DR: Host signaling triggered by TLR and other activating ligands during the course of Yersinia infection redirects both the mechanism of host cell death and the downstream consequences of death by shifting from noninflammatory apoptosis to inflammatory pyroptosis.