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- W2810201809 abstract "Legionella pneumophila elicits caspase-11-driven macrophage pyroptosis through guanylate-binding proteins (GBPs) encoded on chromosome 3. It has been proposed that microbe-driven IFN upregulates GBPs to facilitate pathogen vacuole rupture and bacteriolysis preceding caspase-11 activation. We show here that macrophage death occurred independently of microbial-induced IFN signaling and that GBPs are dispensable for pathogen vacuole rupture. Instead, the host-intrinsic IFN status sustained sufficient GBP expression levels to drive caspase-1 and caspase-11 activation in response to cytosol-exposed bacteria. In addition, endogenous GBP levels were sufficient for the release of DNA from cytosol-exposed bacteria, preceding the cyclic GMP-AMP synthase/stimulator of interferon genes (cGAS/STING) pathway for Ifnb induction. Mice deficient for chromosome 3 GBPs were unable to mount a rapid IL-1/chemokine (C-X-C motif) ligand 1 (CXCL1) response during Legionella-induced pneumonia, with defective bacterial clearance. Our results show that rapid GBP activity is controlled by host-intrinsic cytokine signaling and that GBP activities precede immune amplification responses, including IFN induction, inflammasome activation, and cell death." @default.
- W2810201809 created "2018-07-10" @default.
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- W2810201809 creator A5076382250 @default.
- W2810201809 date "2018-07-01" @default.
- W2810201809 modified "2023-10-15" @default.
- W2810201809 title "Constitutive Interferon Maintains GBP Expression Required for Release of Bacterial Components Upstream of Pyroptosis and Anti-DNA Responses" @default.
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- W2810201809 doi "https://doi.org/10.1016/j.celrep.2018.06.012" @default.
- W2810201809 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6063733" @default.
- W2810201809 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/29972777" @default.
- W2810201809 hasPublicationYear "2018" @default.
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