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• W2398372682 abstract "The yeast Candida albicans causes human infections that have mortality rates approaching 50%. The key to developing improved therapeutics is to understand the host-pathogen interface. A critical interaction is that with macrophages: intracellular Candida triggers the NLRP3/caspase-1 inflammasome for escape through lytic host cell death, but this also activates antifungal responses. To better understand how the inflammasome response to Candida is fine-tuned, we established live-cell imaging of inflammasome activation at single-cell resolution, coupled with analysis of the fungal ERMES complex, a mitochondrial regulator that lacks human homologs. We show that ERMES mediates Candida escape via inflammasome-dependent processes, and our data suggest that inflammasome activation is controlled by the level of hyphal growth and exposure of cell wall components as a proxy for severity of danger. Our study provides the most detailed dynamic analysis of inflammasome responses to a fungal pathogen so far and establishes promising pathogen- and host-derived therapeutic strategies." @default.
• W2398372682 created "2016-06-24" @default.
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• W2398372682 date "2016-06-22" @default.
• W2398372682 modified "2023-10-16" @default.
• W2398372682 title "The Endoplasmic Reticulum-Mitochondrion Tether ERMES Orchestrates Fungal Immune Evasion, Illuminating Inflammasome Responses to Hyphal Signals" @default.
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• W2398372682 doi "https://doi.org/10.1128/msphere.00074-16" @default.
• W2398372682 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4888881" @default.
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• W2398372682 hasPublicationYear "2016" @default.
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