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Autoimmune inflammation causes hematopoietic stem cells to generate a trained immunity program inherited by BMDMs [RNAseq_primary_data]

ABSTRACT: Autoimmune inflammation causes hematopoietic stem cells to generate a trained immunity program inherited by BMDMs [RNAseq_primary_data]

PROVIDER: PRJNA1111868 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29041402_1.fastq.gz	Fastqsanger.gz
	SRR29041402_2.fastq.gz	Fastqsanger.gz
	SRR29041403_1.fastq.gz	Fastqsanger.gz
	SRR29041403_2.fastq.gz	Fastqsanger.gz
	SRR29041404_1.fastq.gz	Fastqsanger.gz

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Autoimmune inflammation causes hematopoietic stem cells to generate a trained immunity program inherited by BMDMs [RNAseq_primary_data]

Project description:Trained immunity occurs when inflammatory stimulation reprograms myeloid cells to have increased effector functions upon secondary stimulation. We found that autoimmune inflammation indiced trained immunity in bone marrow derived macrophages (BMDMs) in mice treated with pristane for eight weeks. We then analyzed the chromatin landscape and transcriptome using low input chromatin accessibility and transcriptomics sequencing (LiCAT-seq) which allows for the co-generation of RNA-seq and ATAC-seq libraries from the same cellular pool. With this approach we found that BMDMs had increased chromatin accessibility at metabolic genes and inflammatory related genes in BMDMs from pristane treated mice, which resulted in increased transcription of metabolic and inflammatory genes, leading to enhanced metabolism and inflammatory functions in BMDMs.

2024-10-15 | GSE267563 | GEO

Autoimmune inflammation causes hematopoietic stem cells to generate a trained immunity program inherited by BMDMs [ATACseq_primary_data]

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Autoimmune inflammation causes hematopoietic stem cells to generate a trained immunity program inherited by BMDMs [RNAseq_secondary_data]

Project description:Autoimmune inflammation causes hematopoietic stem cells to generate a trained immunity program inherited by BMDMs [RNAseq_secondary_data]

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Autoimmune inflammation causes hematopoietic stem cells to generate a trained immunity program inherited by BMDMs [ATACseq_primary_data]

Project description:Autoimmune inflammation causes hematopoietic stem cells to generate a trained immunity program inherited by BMDMs [ATACseq_primary_data]

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Autoimmune inflammation causes hematopoietic stem cells to generate a trained immunity program inherited by BMDMs [ATACseq_secondary_data]

Project description:Autoimmune inflammation causes hematopoietic stem cells to generate a trained immunity program inherited by BMDMs [ATACseq_secondary_data]

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Autoimmune inflammation causes hematopoietic stem cells to generate a trained immunity program inherited by BMDMs [RNAseq_secondary_data]

Project description:Trained immunity occurs when inflammatory stimulation reprograms myeloid cells to have increased effector functions upon secondary stimulation. Interestingly, the secondary stimulation can occur well beyond the lifetime of an individual myeloid cell, thus memory of immune training must reside in the hematopoietic system. After showing that long-term hematopoietic stem cells (HSCLT) from mice treated with pristane for eight weeks generate trained macrophages, we sought to uncover mechanisms underlying the heritable trained immunity program in myeloid cells. To do this we transplanted HSCLT from pristane mice into congenic recipients, and after 18 weeks of engraftment we generated bone marrow derived macrophages (BMDMs) in vitro. We then analyzed the chromatin landscape and transcriptome using low input chromatin accessibility and transcriptomics sequencing (LiCAT-seq) which allows for the co-generation of RNA-seq and ATAC-seq libraries from the same cellular pool. With this approach we found a unique epigenetic phenotype of reduced chromatin accessibility at metabolic genes in BMDMs from pristane HSCLT, which resulted in reduced transcription of metabolic genes, leading to reduced metabolism in BMDMs.

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Autoimmune inflammation causes hematopoietic stem cells to generate a trained immunity program inherited by BMDMs [ATACseq_secondary_data]

Project description:Trained immunity occurs when inflammatory stimulation reprograms myeloid cells to have increased effector functions upon secondary stimulation. Interestingly, the secondary stimulation can occur well beyond the lifetime of an individual myeloid cell, thus memory of immune training must reside in the hematopoietic system. After showing that long-term hematopoietic stem cells (HSCLT) from mice treated with pristane for eight weeks generate trained macrophages, we sought to uncover mechanisms underlying the heritable trained immunity program in myeloid cells. To do this we transplanted HSCLT from pristane mice into congenic recipients, and after 18 weeks of engraftment we generated bone marrow derived macrophages (BMDMs) in vitro. We then analyzed the chromatin landscape and transcriptome using low input chromatin accessibility and transcriptomics sequencing (LiCAT-seq) which allows for the co-generation of RNA-seq and ATAC-seq libraries from the same cellular pool. With this approach we found a unique epigenetic phenotype of reduced chromatin accessibility at metabolic genes in BMDMs from pristane HSCLT, which resulted in reduced transcription of metabolic genes, leading to reduced metabolism in BMDMs.

2024-10-15 | GSE267518 | GEO

RNA-Seq of BMDM from aged mice and the effect of trained immunity

Project description:We generated BMDMs from aged C57BL/6J mice. BMDMs were treated with C.ablican derived β-glucan, which is known to induce trained immunity. mRNA was isolated form immune trained and control BMDMs using the Rneasy Kit from Qiagen. Library preparation and sequencing performed by Novogene. We found that trained immunity induced transcriptional changes in BMDMs from aged mice

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IL-4 induced non-canonical trained immunity in murine BMDMs

Project description:IL-4 induced non-canonical trained immunity in murine BMDMs

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Project description:BMDMs from naïve female FVB mice were used to generate BMDMs which were polarized for 4 hours using either INFG or IL4. These were subjected to polysome-profiling.

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