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RNA sequencing data of microglia, meningeal macrophages (mMΦ) and perivascular macrophages (pvMΦ) isolated from brains of Cx3cr1-GFP mice at different age.

ABSTRACT: All tissue resident macrophages of the central nervous system (CNS), including parenchymal microglia as well as CNS-associated macrophages (CAMs) such as meningeal (mMF) and perivascular macrophages (pvMF) are part of the CNS endogenous innate immune system that acts as the first line of defense during infections or trauma. It has been suggested that microglia and all CAM subsets are derived from prenatal cellular sources in the yolk sac that were defined as early erythromyeloid progenitors. However, the precise ontogenetic relationships, the underlying transcriptional programs and the molecular signals that drive the development of distinct CAMs subsets in situ are poorly understood. Using novel fate mapping systems, single-cell profiling and cell-specific mutants, we show that only mMF and microglia share a common prenatal progenitor. In contrast, pvMF originate from perinatal mMF only after birth in an integrin-dependent manner. Furthermore, the establishment of pvMFcritically requires the presence of vascular smooth muscle cells. In summary, our data reveal a novel precisely timed process in distinct anatomical niches for the establishment of CNS macrophage subsets.

ORGANISM(S): Mus musculus

PROVIDER: GSE194432 | GEO | 2022/01/27

REPOSITORIES: GEO

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RNA sequencing data of CNS-associated macrophages (CAMs) isolated from brains of Mrc1-CreERT2 mice

Project description:All tissue resident macrophages of the central nervous system (CNS), including parenchymal microglia as well as CNS-associated macrophages (CAMs) such as meningeal (mMF) and perivascular macrophages (pvMF) are part of the CNS endogenous innate immune system that acts as the first line of defense during infections or trauma. It has been suggested that microglia and all CAM subsets are derived from prenatal cellular sources in the yolk sac that were defined as early erythromyeloid progenitors. However, the precise ontogenetic relationships, the underlying transcriptional programs and the molecular signals that drive the development of distinct CAMs subsets in situ are poorly understood. Using novel fate mapping systems, single-cell profiling and cell-specific mutants, we show that only mMF and microglia share a common prenatal progenitor. In contrast, pvMF originate from perinatal mMF only after birth in an integrin-dependent manner. Furthermore, the establishment of pvMF critically requires the presence of vascular smooth muscle cells. In summary, our data reveal a novel precisely timed process in distinct anatomical niches for the establishment of CNS macrophage subsets.

2022-01-27 | GSE194433 | GEO

Specification of CNS macrophage subsets occurs postnatally in defined anatomical niches

Project description:All tissue resident macrophages of the central nervous system (CNS), including parenchymal microglia as well as CNS-associated macrophages (CAMs) such as meningeal (mMF) and perivascular macrophages (pvMF) are part of the CNS endogenous innate immune system that acts as the first line of defense during infections or trauma. It has been suggested that microglia and all CAM subsets are derived from prenatal cellular sources in the yolk sac that were defined as early erythromyeloid progenitors. However, the precise ontogenetic relationships, the underlying transcriptional programs and the molecular signals that drive the development of distinct CAMs subsets in situ are poorly understood. Using novel fate mapping systems, single-cell profiling and cell-specific mutants, we show that only mMF and microglia share a common prenatal progenitor. In contrast, pvMF originate from perinatal mMF only after birth in an integrin-dependent manner. Furthermore, the establishment of pvMF critically requires the presence of vascular smooth muscle cells. In summary, our data reveal a novel precisely timed process in distinct anatomical niches for the establishment of CNS macrophage subsets.

2022-01-26 | GSE195437 | GEO

HOST MICROBIOTA REGULATE SELECTIVE MYELOID SUBSETS IN THE CENTRAL NERVOUS SYSTEM DURING HOMEOSTASIS AND DISEASE

Project description:The immune cells of the central nervous system (CNS) comprise parenchymal microglia and at the CNS border regions meningeal, perivascular and choroid plexus macrophages (summarized as CNS-associated macrophages, CAMs). Previous work has uncovered that microglial properties are strongly dependent on environmental signals from the commensal microbiota while its effect on CAMs remained unknown. By combining several microbiota manipulation approaches, genetic mouse models and single-cell RNA-sequencing, we comprehensively characterized CNS myeloid cell composition and function. Under steady-state, the transcriptional profile and numbers of choroid plexus macrophages were found to be tightly steered by complex microbiota. Divergently, perivascular and meningeal macrophages were affected to a lesser extent. An acute perturbation through viral infection evoked an attenuated immune response of all CAMs in germ-free mice. Additionally, we assessed CAMs in a more chronic pathological state in 5xFAD mice as a model for Alzheimer’s disease whereby exclusively perivascular macrophages displayed enhanced amyloid beta uptake in GF 5xFAD mice. Our results provide novel insights for understanding distinct microbiota-CNS macrophage interactions during health and perturbation that could potentially be targeted therapeutically.

2021-10-01 | GSE178956 | GEO

Cell-autonomous effects of APOE4 in restricting microglial response in brain homeostasis and Alzheimer’s disease

Project description:Cells in the cortex of mice expressing apoE3 or apoE4 in the microglia were isolated and subjected to the single-cell RNA seq to investigate the effects of microglia/CNS-associated macrophages (CAMs) apoE on the brain transcriptomic profiles. Our data revealed that microglia/CAM-expressed apoE3 promotes antigen presentation and immune patnways, whereas apoE4 down-regulates complement and promotes stress-related responses.

2023-11-02 | GSE241553 | GEO

Effect of peripherally-derived macrophages in adult microglia (mouse cells)

Project description:Infiltrating monocyte derived macrophages (MDMs) and resident microglia dominate CNS injury sites. We show that MDMs and microglia can directly communicate to modulate each other’s function. Also, the presence of MDMs in CNS injury suppresses microglia-mediated phagocytosis and inflammation. We suggest that macrophages infiltrating the injured CNS provide a mechanism to control acute and chronic microglia-mediated inflammation, which could otherwise drive damage in a variety of CNS conditions. To understand the global effects of macrophage communication to microglia, we transcriptionally profiled activated adult mouse microglia in the presence or absence of macrophages with and without an inflammatory stiumulus (LPS)

2018-08-01 | GSE102482 | GEO

Expression data from polarized adult human macrophages

Project description:Myeloid cells are prominent cellular constituents of the CNS. Under physiologic conditions, these include microglia within the parenchyma and systemic compartment derived macrophages localized to the perivascular spaces. Defining the relative distribution and functions of microglia versus blood-derived macrophages in the CNS parenchyma under pathologic conditions remains a challenge due to limitations in being able to distinguish these cell types. Approaches to distinguishing microglia and macrophages in experimental models include use of chimeric and parabiotic animals and molecular genetic techniques to selectively differentially label or delete a specific cell type. The current report will compare gene expression of human microglia and macrophages under distinct states of activation or “polarization” and relate these to their roles in tissue injury and protection /repair in the central nervous system (CNS). We used Affymetrix Human Gene HT 2.0 microarrays to compare whole transcriptomes of microglia and macrophages under defined polarization conditions.

2016-02-01 | GSE76736 | GEO

AffyExon1 genearray expression profile of adult mouse microglia and splenic Ly6C monocytes

Project description:Gene profiling of CNS-derived microglia vs splenic CD11b+Ly6C+ monocyte subsets deom adult mice Gene array identified 1572 genes that were enriched in microglia vs. 611 monocyte enriched genes with a greater than 5-fold difference (P<0.001). Gene profiling of CD11b+CD45Low microglia isolated from the CNS and CD11b+Ly6C+ monocyte subsets isolated from the spleen of naM-CM-/ve adult mice.

2013-07-08 | E-GEOD-48579 | biostudies-arrayexpress

Transcriptomes of Tgfbr2 Knockout Microglia and Macrophages

Project description:The cytokine transforming growth factor-B (TGF-B) regulates development and homeostasis of several tissue-resident macrophage populations, including microglia. TGF-B is not critical for microglia survival, but is required for the maintenance of the microglia-specific homeostatic gene signature. Under defined host conditions circulating monocytes can compete for the microglial niche and give rise to long-lived monocyte-derived macrophages residing in the central nervous system (CNS). Whether monocytes require TGF-B for colonization of the microglial niche and maintenance of CNS integrity is unknown. We found that abrogation of TGF-B signaling in CX3CR1+ monocyte-derived macrophages led to rapid onset of a progressive and fatal demyelinating motor disease characterized by myelin-laden giant macrophages throughout the spinal cord. The devastating motor disease that developed in TGF-BR2-deficient chimeras indicated that in the absence of TGF-B signaling the CNS environment licenses monocyte-derived macrophages for tissue damage. We therefore addressed how the gene expression signature of CNS macrophages was controlled by TGF-B signaling. We thus sorted TGF-BR2-deficient monocyte-derived macrophages from animals with ongoing motor disease and from their wildtype littermate counterparts. For comparison we sorted wild-type and TGF-BR2-deficient microglia and performed RNA sequencing for all four groups. Tgfbr2-deficient macrophages were characterized by high expression of genes encoding proteins involved in antigen presentation, inflammation and phagocytosis. TGF-B is thus crucial for the functional integration of monocytes into the CNS microenvironment.

2018-04-16 | GSE111385 | GEO

Multiomic spatial landscape of innate immune cells at human central nervous system borders

Project description:The innate immune system of the human central nervous system (CNS) is highly diverse already during homeostasis. Several immune cell populations such as macrophages that are frequent in the brain parenchyma (microglia) and less numerous at the brain interfaces as CNS-associated macrophages (CAMs) constitute the local immune compartment. Due to their scantiness and particular location, little is known about the presence of temporally and spatially restricted CAM subclasses during development, health and perturbation. Here, we combined several high-dimensional technologies, such as single-cell RNA-sequencing, time-of-flight mass cytometry and single-cell spatial transcriptomics with fate mapping and advanced immunohistochemistry to comprehensively characterize the immune system at human CNS interfaces. We also provide a comprehensive analysis of resident and engrafted myeloid cells in the brains of individuals with peripheral blood stem cell transplantation, revealing remarkable dynamics. These approaches enabled us to identify a previously unappreciated spectrum of transcriptional classes of human CAMs and to decipher their turnover with circulating cells. CAM signatures profoundly changed during ontogeny and pathology. Our results highlight myeloid diversity at the interfaces of the human CNS with the periphery and provide new insights into the human brain’s immune system.

2023-12-20 | GSE245311 | GEO

RNA sequencing of microglia sorted form tamoxifen treated Sall1CreER/fl and control Sall1fl/fl mice

Project description:Microglia are the resident macrophages of the central nervous system (CNS). Gene profiling identified the transcriptional regulator Sall1 as a microglia signature gene. Given the high expression of Sall1 in microglia, we sought to identify its function in vivo. The Sall1CreER allele has been targeted into the Sall1 locus, therefore Sall1CreER/fl mice (heterozygous for both alleles) allow inducible ablation of Sall1 expression in microglia after tamoxifen treatment. We performed RNA-seq to examine gene expression profiles of microglia sorted from tamoxifen treated adult Sall1CreER/fl mice and Sall1fl/fl control littermates. Microglia were obtained with > 98% purity and the absence of Sall1 was confirmed in Sall1CreER/fl microglia. We could show that deletion of Sall1 in microglia in vivo resulted in the conversion of these cells from resting tissue macrophages into inflammatory phagocytes leading to altered neurogenesis and disturbed tissue homeostasis. Similar changes in gene expression profiles were found in Sall1-deficient microglia isolated from tamoxifen-treated Cx3cr1CreERSall1fl/fl mice. In these mice, deletion of Sall1 is targeted to CX3CR1+ myeloid cells including microglia and CNS-associated macrophages but not to any other CNS-resident cells. This indicated that Sall1 transcriptional regulation maintains microglia identity and physiological properties in the CNS.

2016-10-19 | E-MTAB-5077 | biostudies-arrayexpress

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