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

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

PROVIDER: PRJNA957725 | 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 [ChIPseq]

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

| PRJNA957727 | ENA

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

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

| PRJNA957721 | ENA

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

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.

2024-05-17 | GSE230141 | GEO

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

2024-05-17 | GSE230138 | GEO

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

Project description: Not available

| S-EPMC11219877 | biostudies-literature

Histone H3 lysine 9 di-methylation as an epigenetic signature of the interferon response

Project description:This SuperSeries is composed of the following subset Series: GSE22102: Histone H3 lysine 9 di-methylation as an epigenetic signature of the interferon response (sequencing) GSE24774: Histone H3 lysine 9 di-methylation as an epigenetic signature of the interferon response (WT and G9a deficient DCs) GSE24776: Histone H3 lysine 9 di-methylation as an epigenetic signature of the interferon response (WT and G9a deficient MEFs) Refer to individual Series

2012-03-02 | E-GEOD-24826 | biostudies-arrayexpress

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

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-05-17 | GSE230142 | GEO

Histone H3 Lysine 4 mono-, di- and trimethyl and CTCF in CD4+CD25+CD45RA+ regulatory and conventional CD4+CD25- T-cells

Project description:Analysis of Histone H3 Lysine 4 mono-, di- and trimethyl and the boundary protein CTCF in CD4+CD25+CD45RA+ regulatory T-cells and conventional CD4+CD25- T-cells. To investigate regulatory functions or potential new transcription start sites in Treg and Tconv cells, we investigated the associated histone modifications. Mono- and dimethylation of histone 3 lysin 4 (H3K4) were previously shown to mark enhancer regions, whereas H3K4 trimethylation generally associates with transcription start sites. At imprinted loci, binding of the insulator protein CTCF, which restricts or directs enhancer-promoter interactions, is often regulated by DNA-methylation. Therefore we performed ChIP-on-chip experiments (chromatin immunoprecipitation followed by microarray hybridization; samples were amplified with ligation mediated PCR [see label protocol for the procedure] prior to labeling) for mono- di- and trimethylation of histone 3 lysin 4 and of CTCF in expanded Treg and Tconv cells. Keywords: ChIP-on-chip ChIP-on-chip experiments for H3K4 mono-, di- and trimethyl and CTCF in CD4+CD25+CD45RA+ regulatory T-cells and conventional CD4+CD25- T-cells were co-hybridizied with the input. Three biologiacal replicates (rep1-3) were performed for every histone mark, two CTCF (rep1 and rep2).

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Tissue-resident memory T cells maintain identity after in vitro restimulation

Project description:Resident memory T (TRM) cells have been recently established as an important subset of memory cells that provide early and essential protection against reinfection in the absence of circulating memory T cells. Recent findings showing that TRM expand in vivo after repeated antigenic stimulation indicate that these memory T cells are not terminally differentiated. This suggest an opportunity for in vitro TRM expansion to apply in an immunotherapy setting. However, it has also been shown that TRM may not maintain their identity and form circulating memory T cells after in vivo restimulation. Therefore, we set out to determine how TRM respond to antigenic activation in culture. Using Listeria monocytogenes and LCMV infection models, we found that TRM from the intraepithelial compartment of the small intestine expand in vitro after antigenic stimulation and subsequent resting in homeostatic cytokines. A large fraction of the expanded TRM retained their phenotype, including the expression of key TRM markers CD69 and CD103 (ITGAE). Optimal culture of TRM required low O2 pressure to maintain the expression of these and other TRM associated molecules. Expanded TRM retained their effector capacity to produce cytokines after restimulation, but did not acquire a highly glycolytic profile indicative of effector T cells. Proteomic analysis confirmed TRM profile retention, including expression of TRM-related transcription factors, tissue retention factors, adhesion molecules and enzymes involved in fatty acid metabolism. Collectively, our data indicate that limiting oxygen conditions support in vitro expansion of TRM cells that maintain their TRM phenotype, at least in part, suggesting an opportunity for therapeutic strategies that require in vitro expansion of TRM.

2025-09-30 | PXD041211 | Pride

Histone H3 Lysine 4 mono-, di- and trimethyl and CTCF in CD4+CD25+CD45RA+ regulatory and conventional CD4+CD25- T-cells

2009-05-20 | GSE14234 | GEO