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

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

PROVIDER: PRJNA957727 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24225809.fastq.gz	Fastqsanger.gz
	SRR24225810.fastq.gz	Fastqsanger.gz
	SRR24225811.fastq.gz	Fastqsanger.gz
	SRR24225812.fastq.gz	Fastqsanger.gz
	SRR24225813.fastq.gz	Fastqsanger.gz

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

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

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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.

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