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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE267569 | GEO | 2024/10/15

REPOSITORIES: GEO

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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

Impact of autoimmune inflammation on HSPC and monocyte gene expression

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 sorted out donor derived granulocyte monocyte progenitors (GMP). 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 GMP from pristane HSCLT, which resulted in reduced transcription of metabolic genes, leading to reduced metabolism in mature macrophages.

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Impact of HSC-derived immune training on granulocyte/macrophage progenitor gene expression

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 sorted out donor derived granulocyte monocyte progenitors (GMP). 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 GMP from pristane HSCLT, which resulted in reduced transcription of metabolic genes, leading to reduced metabolism in mature macrophages.

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Impact of HSC-derived immune training on granulocyte/macrophage progenitor chromatin landscape

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 sorted out donor derived granulocyte monocyte progenitors (GMP). 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 GMP from pristane HSCLT, which resulted in reduced transcription of metabolic genes, leading to reduced metabolism in mature macrophages.

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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.

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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 | GSE267516 | GEO

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Project description:Increased number of circulating myeloid cells is a hallmark of several cancers, however it remains unclear how primary tumors impact on myelopoiesis. Here we show that non-metastatic breast tumors remotely instruct the fate of long-term hematopoietic stem cell (HSCLT) in the bone marrow. We found that HSCLT from tumor bearing mice acquire a myeloid bias persisting upon primary and secondary HSCLT transfer in lethally-irradiated tumor-free animals. By imaging the bone marrow HSC niche, we found that the tumor-bearing status is associated with increased physical interactions between mesenchymal stem/stromal cells (MSC) and HSCLT. Moreover, ex vivo co-culture experiments demonstrate that MSC isolated from tumor-bearing mice increase myeloid differentiation of HSCLT isolated from tumor free mice. In summary, our data reveal that breast cancer remotely promotes myelopoiesis at the earliest stages of hematopoietic differentiation in the bone marrow mesenchymal niche.

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