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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE267516 | 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 [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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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

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.

2024-10-15 | GSE267569 | GEO

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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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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.

2024-10-15 | GSE205482 | GEO

Genomic features enabling control of inflammatory gene expression by antagonistic signals

Project description:BMDMs or iMACs were generated via differentiation of bone marrow cells or immortalized precursors, respectively, in culture media containing m-CSF for 7 day. Upon differentiation, BMDMs or iMacs were left untreated or stimulated as described below. 1) BMDM WT were stimulated with LPS, PGE2, IL-10, LPS+PGE2, LPS+IL-10 for 4 hours: each condition in triplicate. This experiment was performed to assess chromatin accessibility in the concomitant presence of pro-inflammatory (LPS) and anti-inflammatory stimuli (PGE2 and IL-10). 2) MEF2A-deficient iMac clones (D7, A7, A8, C7) and MEF2A-proficient (referred to as wild-type) iMac clones (NE, B3 and D10) were generated via CRISPR/Cas9 and stimulated or not with LPS for either 4 hours: each condition in single. This experiment was performed to assess the role in MEF2a in controlling chromatin accessibility upon LPS stimulation.

2021-06-08 | E-MTAB-9252 | biostudies-arrayexpress

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

2022-03-12 | GSE198083 | GEO

Effect of SWI/SNF pertubations on chromatin accessibility during macrophage inflammatory activation [ATAC-seq]

Project description:To understand how macrophage chromatin respond to LipidA stimulation, we profiled accessibility for WT BMDMs with 0hr, 1hr, or 4hr LipidA stimulation. In addition, we also profiled accessibility for WT BMDMs treated with ACBI1, BRM014, BRDK98, or dBrd9 and for Arid1A-/- Pbrm1-/- BMDMs after 0hr, 1hr, or 4hr LipidA stimulation.

2024-06-05 | GSE242799 | GEO

Uremic toxin indoxyl sulfate induces trained immunity via the AhR-dependent arachidonic acid pathway in end-stage renal disease [RNAseq]

Project description:Trained immunity is the long-term functional reprogramming of innate immune cells, which results in altered responses toward a secondary challenge. Despite indoxyl sulfate (IS) being a potent stimulus associated with chronic kidney disease (CKD)-related inflammation, its impact on trained immunity has not been explored. Here, we demonstrate that IS induces trained immunity in monocytes via epigenetic and metabolic reprogramming, resulting in augmented cytokine production. Mechanistically, the aryl hydrocarbon receptor (AhR) contributes to IS-trained immunity by enhancing the expression of arachidonic acid (AA) metabolism-related genes such as Arachidonate 5-Lipoxygenase (ALOX5) and ALOX5 Activating Protein (ALOX5AP). Inhibition of AhR during IS training suppresses the induction of IS-trained immunity. Monocytes from end-stage renal disease (ESRD) patients have increased ALOX5 expression and after 6-day training, they exhibit enhanced TNF-α and IL-6 production to LPS. Furthermore, healthy control-derived monocytes trained with uremic sera from ESRD patients exhibit increased production of TNF-α and IL-6. Consistently, IS-trained mice and their splenic myeloid cells had increased production of TNF-α after in vivo and ex vivo LPS stimulation compared to that of control mice. These results provide insight into the role of IS in the induction of trained immunity, which is critical during inflammatory immune responses in CKD patients.

2024-06-20 | GSE263024 | GEO

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