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- W4313360106 abstract "Abstract Many bacteria require entrance into host immune cells, such as macrophages, in order to replicate. These intracellular bacteria have evolved complex strategies for avoiding the antimicrobial programming of these immune cells to create replicative niches. While we know a great deal about various virulence factors deployed by intracellular bacteria as well as how cells try to kill these pathogens, how bacteria and host cells modulate each others’ responses during infection is less well understood. Using the Gram-negative bacteria Burkholderia cenocepacia, we have uncovered a negative relationship between type I IFN signaling and the replicative potential of invading bacteria. Firstly, cells infected with these bacteria produce significant levels of IFN as well as the products of IFN-stimulated genes (ISGs). Cells pre-treated with IFNβ are less permissive to bacterial replication, while cells from mice lacking the type I IFN receptor (IFNAR) have increased levels of bacterial replication compared to wild-type cells. Interestingly, this phenotype is type I IFN-specific, as pre-treatment with IFNγ has no effect on bacterial replication. Additionally, siRNA knockdown of select ISGs, such as IFIT1, leads to increased bacterial replication within macrophages. A rigorous, concurrent transcriptomic profiling of both infected cells and intracellular bacteria is providing insight into how the bacteria and their host cells interact with one another during acute infection, providing a basis for targeted CRISPR-based screening experiments to unravel critical regulators of the host-pathogen interaction." @default.
- W4313360106 created "2023-01-06" @default.
- W4313360106 creator A5017515840 @default.
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- W4313360106 date "2017-05-01" @default.
- W4313360106 modified "2023-09-25" @default.
- W4313360106 title "Type I IFN mediates cell-intrinsic host protective effects during acute gram-negative bacterial infection of macrophages" @default.
- W4313360106 doi "https://doi.org/10.4049/jimmunol.198.supp.123.7" @default.
- W4313360106 hasPublicationYear "2017" @default.
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