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The epigenetic regulator Histone Deacetylase 3 regulates the ontogeny and maintenance of tissue-resident macrophage

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE122533 | GEO | 2020/06/23

REPOSITORIES: GEO

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The epigenetic regulator Histone Deacetylase 3 regulates the ontogeny and maintenance of tissue-resident macrophage [scRNA-Seq]

Project description:Tissue-resident macrophages (TRMs) play central roles in local tissue development and immunity. However, how to control TRM ontogeny and maintenance remains unclear. We performed transcriptional and histone modification analyses of alveolar macrophages in mice with myeloid-specific (Csf1rCre) deletion of HDAC3 using bulk RNA-seq, single-cell RNA-seq and ChIP-seq. We report that HDAC3 deficiency results in metabolic disorders and increased cell death of the fetal lung TRMs, which is partially regulated through directly targeting PPAR-γ. Although the loss of AMs in the absence of HDAC3 is not AM subset specific, the transcriptome changes in HDAC3 deficient AM subsets are different. We propose that HDAC3 serves a key epigenetic regulator that controls embryonic TRM ontogeny and maintenance.

2020-09-22 | GSE122529 | GEO

The epigenetic regulator Histone Deacetylase 3 regulates the ontogeny and maintenance of tissue-resident macrophage [ChIP-Seq]

2020-06-23 | GSE122532 | GEO

The epigenetic regulator Histone Deacetylase 3 regulates the ontogeny and maintenance of tissue-resident macrophage [RNA-Seq]

2020-06-23 | GSE122393 | GEO

The epigenetic regulator Histone Deacetylase 3 regulates the ontogeny and maintenance of tissue-resident macrophage

Project description:The epigenetic regulator Histone Deacetylase 3 regulates the ontogeny and maintenance of tissue-resident macrophage

| PRJNA505491 | ENA

The epigenetic regulator Histone Deacetylase 3 regulates the ontogeny and maintenance of tissue-resident macrophage [RNA-Seq]

Project description:The epigenetic regulator Histone Deacetylase 3 regulates the ontogeny and maintenance of tissue-resident macrophage [RNA-Seq]

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The epigenetic regulator Histone Deacetylase 3 regulates the ontogeny and maintenance of tissue-resident macrophage [scRNA-Seq]

Project description:The epigenetic regulator Histone Deacetylase 3 regulates the ontogeny and maintenance of tissue-resident macrophage [scRNA-Seq]

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The epigenetic regulator Histone Deacetylase 3 regulates the ontogeny and maintenance of tissue-resident macrophage [ChIP-Seq]

Project description:The epigenetic regulator Histone Deacetylase 3 regulates the ontogeny and maintenance of tissue-resident macrophage [ChIP-Seq]

| PRJNA505496 | ENA

The microbial metabolite butyrate regulates intestinal macrophage function via histone deacetylase inhibition.

Project description:Given the trillions of microbes that inhabit the mammalian intestines, the host immune system must constantly maintain a balance between tolerance to commensals and immunity against pathogens to avoid unnecessary immune responses against otherwise harmless bacteria. Misregulated responses can lead to inflammatory bowel diseases such as ulcerative colitis or Crohn's disease. The mechanisms by which the immune system maintains this critical balance remain largely undefined. Here, we demonstrate that the short-chain fatty acid n-butyrate, which is secreted in high amounts by commensal bacteria, can modulate the function of intestinal macrophages, the most abundant immune cell type in the lamina propria. Treatment of macrophages with n-butyrate led to the down-regulation of lipopolysaccharide-induced proinflammatory mediators, including nitric oxide, IL-6, and IL-12, but did not affect levels of TNF-? or MCP-1. These effects were independent of toll-like receptor signaling and activation of G-protein-coupled receptors, two pathways that could be affected by short-chain fatty acids. In this study, we provide several lines of evidence that suggest that these effects are due to the inhibition of histone deacetylases by n-butyrate. These findings elucidate a pathway in which the host may maintain tolerance to intestinal microbiota by rendering lamina propria macrophages hyporesponsive to commensal bacteria through the down-regulation of proinflammatory effectors.

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Epigenetic Control of Macrophage Shape Transition towards an Atypical Elongated Phenotype by Histone Deacetylase Activity.

Project description:Inflammatory chronic pathologies are complex processes characterized by an imbalance between the resolution of the inflammatory phase and the establishment of tissue repair. The main players in these inflammatory pathologies are bone marrow derived monocytes (BMDMs). However, how monocyte differentiation is modulated to give rise to specific macrophage subpopulations (M1 or M2) that may either maintain the chronic inflammatory process or lead to wound healing is still unclear. Considering that inhibitors of Histone Deacetylase (HDAC) have an anti-inflammatory activity, we asked whether this enzyme would play a role on monocyte differentiation into M1 or M2 phenotype and in the cell shape transition that follows. We then induced murine bone marrow progenitors into monocyte/macrophage differentiation pathway using media containing GM-CSF and the HDAC blocker, Trichostatin A (TSA). We found that the pharmacological inhibition of HDAC activity led to a shape transition from the typical macrophage pancake-like shape into an elongated morphology, which was correlated to a mixed M1/M2 profile of cytokine and chemokine secretion. Our results present, for the first time, that HDAC activity acts as a regulator of macrophage differentiation in the absence of lymphocyte stimuli. We propose that HDAC activity down regulates macrophage plasticity favoring the pro-inflammatory phenotype.

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The lymphoid-associated interleukin 7 receptor (IL7R) regulates tissue-resident macrophage development.

Project description:The discovery of a fetal origin for tissue-resident macrophages (trMacs) has inspired an intense search for the mechanisms underlying their development. Here, we performed in vivo lineage tracing of cells with an expression history of IL7Rα, a marker exclusively associated with the lymphoid lineage in adult hematopoiesis. Surprisingly, we found that Il7r-Cre labeled fetal-derived, adult trMacs. Labeling was almost complete in some tissues and partial in others. The putative progenitors of trMacs, yolk sac (YS) erythromyeloid progenitors, did not express IL7R, and YS hematopoiesis was unperturbed in IL7R-deficient mice. In contrast, tracking of IL7Rα message levels, surface expression, and Il7r-Cre-mediated labeling across fetal development revealed dynamic regulation of Il7r mRNA expression and rapid upregulation of IL7Rα surface protein upon transition from monocyte to macrophage within fetal tissues. Fetal monocyte differentiation in vitro produced IL7R+ macrophages, supporting a direct progenitor-progeny relationship. Additionally, blockade of IL7R function during late gestation specifically impaired the establishment of fetal-derived trMacs in vivo These data provide evidence for a distinct function of IL7Rα in fetal myelopoiesis and identify IL7R as a novel regulator of trMac development.

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