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• W1991442992 endingPage "e1000488" @default.
• W1991442992 startingPage "e1000488" @default.
• W1991442992 abstract "Intracellular bacteria have evolved mechanisms that promote survival within hostile host environments, often resulting in functional dysregulation and disease. Using the Anaplasma phagocytophilum-infected granulocyte model, we establish a link between host chromatin modifications, defense gene transcription and intracellular bacterial infection. Infection of THP-1 cells with A. phagocytophilum led to silencing of host defense gene expression. Histone deacetylase 1 (HDAC1) expression, activity and binding to the defense gene promoters significantly increased during infection, which resulted in decreased histone H3 acetylation in infected cells. HDAC1 overexpression enhanced infection, whereas pharmacologic and siRNA HDAC1 inhibition significantly decreased bacterial load. HDAC2 does not seem to be involved, since HDAC2 silencing by siRNA had no effect on A. phagocytophilum intracellular propagation. These data indicate that HDAC up-regulation and epigenetic silencing of host cell defense genes is required for A. phagocytophilum infection. Bacterial epigenetic regulation of host cell gene transcription could be a general mechanism that enhances intracellular pathogen survival while altering cell function and promoting disease." @default.
• W1991442992 created "2016-06-24" @default.
• W1991442992 creator A5062903958 @default.
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• W1991442992 date "2009-06-19" @default.
• W1991442992 modified "2023-10-16" @default.
• W1991442992 title "Epigenetic Silencing of Host Cell Defense Genes Enhances Intracellular Survival of the Rickettsial Pathogen Anaplasma phagocytophilum" @default.
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• W1991442992 doi "https://doi.org/10.1371/journal.ppat.1000488" @default.
• W1991442992 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2694362" @default.
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