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Epithelial cells maintain memory of prior infection with Streptococcus pneumoniae through di-methylation of histone H3

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE230142 | GEO | 2024/05/17

REPOSITORIES: GEO

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Epithelial cells maintain memory of prior infection with Streptococcus pneumoniae through di-methylation of histone H3.

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Epithelial cells maintain memory of prior infection with Streptococcus pneumoniae through di-methylation of histone H3 [Affymetrix]

Project description:Epithelial cells are the first point of contact for bacteria entering the respiratory tract. Streptococcus pneumoniae is an obligatory human pathobiont of the nasal mucosa, carried asymptomatically but also the cause of severe pneumoniae. The role of the epithelium in maintaining homeostatic interactions or mounting an inflammatory response to invasive S. pneumoniae is currently poorly understood. However, studies have shown that chromatin modifications, at the histone level, induced by bacterial pathogens interfere with the host transcriptional program and promote infection. In this study, we demonstrate that S. pneumoniae actively induces di-methylation of histone H3 on lysine 4 (H3K4me2), which persists for at least 9 days upon clearance of bacteria with antibiotics. We show that infection establishes a unique epigenetic program affecting the transcriptional response of epithelial cells, rendering them more permissive upon secondary infection. Our results establish H3K4me2 as a unique modification induced by infection, distinct from H3K4me3, which localizes to enhancer regions genome-wide. Therefore, this study reveals evidence that bacterial infection leaves a memory in epithelial cells after bacterial clearance, in an epigenomic mark, thereby altering cellular responses for subsequent infections. Transcriptome analysis aimed at testing whether cells respond differently in the primary (1°) and secondary (2°) infection. Differential gene expression and gene set enrichment analysis performed.

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Epithelial cells maintain memory of prior infection with Streptococcus pneumoniae through di-methylation of histone H3 [ChIPseq]

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Project description:Epithelial cells maintain memory of prior infection with Streptococcus pneumoniae through di-methylation of histone H3

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Project description:Streptococcus pneumoniae harbors two cyclic di-AMP (c-di-AMP) phosphodiesterases Pde1 and Pde2. Previously, we demonstrated that deletion of one or both of these proteins leads to growth retardation in culture media, defects in the bacterial stress response, and attenuation in mouse models of disease. All of these phenotypes are due to increased levels of c-di-AMP, since the nature and break down products of each protein are different, and mutations that lower c-di-AMP levels partially restore growth and stress tolerance in these mutants. However, how c-di-AMP mediates pneumococcal stress resistance and virulence is unknown. To establish how c-di-AMP affects the transcriptome, RNA-Seq analysis was employed to compare gene expression between wild-type and Δpde1Δpde2 (ST2734) pneumococci. Overall, the competence regulon was upregulated in the Δpde1Δpde2 mutant.

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