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Monocytes transition to monocyte-macrophages within the inflamed vasculature via CCR2 on monocytes and endothelial TNFR2

ABSTRACT: Monocytes transition to monocyte-macrophages within the inflamed vasculature via CCR2 on monocytes and endothelial TNFR2

PROVIDER: PRJNA806976 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18026734.fastq.gz	Fastqsanger.gz
	SRR18026735.fastq.gz	Fastqsanger.gz
	SRR18026736.fastq.gz	Fastqsanger.gz
	SRR18026737.fastq.gz	Fastqsanger.gz
	SRR18026738.fastq.gz	Fastqsanger.gz

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Monocytes transition to monocyte-macrophages within the inflamed vasculature via CCR2 on monocytes and endothelial TNFR2

Project description:Our study reports that CCR2 dependent functional specialization of monocytes into immature macrophages occurs within the TNF-TNFR2 activated vasculature and establishes a chemokine-based autocrine, feed-forward loop that may aplify the inflammation and renal injury.

2022-02-21 | GSE196730 | GEO

Monocytes transition to monocyte-macrophages within the inflamed vasculature via CCR2 on monocytes and endothelial TNFR2

Project description:Our study reports the CCR2 dependent functional specialization of monocytes into immature macrophages occurs within the TNF-TNFR2 activated vasculature and establishes a chemokine-based autocrine, feed-forward loop that may aplify the inflammation and renal injury.

2022-02-19 | GSE196930 | GEO

Monocytes transition to monocyte-macrophages within the inflamed vasculature via CCR2 on monocytes and endothelial TNFR2

Project description:Monocytes transition to monocyte-macrophages within the inflamed vasculature via CCR2 on monocytes and endothelial TNFR2

| PRJNA807800 | ENA

Monocytes transition to macrophages within the inflamed vasculature via monocyte CCR2 and endothelial TNFR2.

Project description:Monocytes undergo phenotypic and functional changes in response to inflammatory cues, but the molecular signals that drive different monocyte states remain largely undefined. We show that monocytes acquire macrophage markers upon glomerulonephritis and may be derived from CCR2+CX3CR1+ double-positive monocytes, which are preferentially recruited, dwell within glomerular capillaries, and acquire proinflammatory characteristics in the nephritic kidney. Mechanistically, the transition to immature macrophages begins within the vasculature and relies on CCR2 in circulating cells and TNFR2 in parenchymal cells, findings that are recapitulated in vitro with monocytes cocultured with TNF-TNFR2-activated endothelial cells generating CCR2 ligands. Single-cell RNA sequencing of cocultures defines a CCR2-dependent monocyte differentiation path associated with the acquisition of immune effector functions and generation of CCR2 ligands. Immature macrophages are detected in the urine of lupus nephritis patients, and their frequency correlates with clinical disease. In conclusion, CCR2-dependent functional specialization of monocytes into macrophages begins within the TNF-TNFR2-activated vasculature and may establish a CCR2-based autocrine, feed-forward loop that amplifies renal inflammation.

| S-EPMC9006314 | biostudies-literature

Transcriptome comparison between CCR2+ and CCR2- classical monocytes in SIV-infected Macaca nemestrina

Project description:Monocytes have been categorized in three main subpopulations based on CD14 and CD16 surface expression. Classical monocytes are the most abundant subset in the blood. They express a CD14+CD16-CCR2+ phenotype, which confers on them the ability to migrate to inflammatory sites by quickly responding to CCL2 signaling. Here we identified and characterized the surge and expansion of a novel monocyte subset during SIV and HIV infection. They were undistinguishable from classical monocytes regarding CD14 and CD16 expression, but did not express surface CCR2. Transcriptome analysis of sorted cells confirmed that they represent a distinct subpopulation that expresses lower levels of inflammatory cytokines and activation markers than their CCR2+ counterparts. They exhibited impaired phagocytosis and deficient chemotaxis in response to CCL2 and CCL7, besides being refractory to SIV infection. We named these cells atypical CCR2- classical (ACC) monocytes, and believe they play an important role in AIDS pathogenesis, possibly reflecting an anti-inflammatory response against the extreme immune activation observed during SIV and HIV infection. Antiretroviral therapy caused this population to decline in both macaque and human subjects, suggesting that this atypical phenotype may be induced by viral replication. Expression profiling by NanoString nCounter gene expression system. Classical monocytes (CD14++CD16-) from six SIV-infected macaques (day 14 post inoculation) were sorted in two groups according to CCR2 expression.

2012-03-01 | E-GEOD-27559 | biostudies-arrayexpress

Transcriptome comparison between CCR2+ and CCR2- classical monocytes in SIV-infected Macaca nemestrina

2012-03-01 | GSE27559 | GEO

Transcriptomic profiling of lung monocytes and macrophages in mice

Project description:We developed a simplified flow cytometry strategy in order to discriminate monocytes and macrophages in the lung of C57BL/6 mice. Using this strategy, we identified autofluorescent F4/80+ CD11c+ alveolar macrophages, non-autofluorescent CD64+Ly-6C- interstitial macrophages and Ly-6Chi monocytes residing in the lung of WT mice. A fraction of these Ly-6Chi monocytes corresponded to classical blood monocytes associated with the lung vasculature, but another fraction did not depend on CCR2, the chemokine receptor required for monocytes to egress from the bone marrow, as a population of lung Ly-6Chi monocytes was also present in the lung of Ccr2-/- mice. A remaining question was whether lung monocytes represented a particular population of monocytes that could be distinguishable from the classical CCR2-dependent blood monocytes. To address this issue, we performed a transcriptomic comparison of Ly-6Chi monocytes recovered from flushed lung of WT mice (â60% of CCR2- dependent classical blood monocytes and â40% of lung monocytes) and Ccr2-/- mice (more than 95% of lung monocytes). In addition, we tested whether exposure to TLR ligands would affect interstitial macrophages, and we compared to transcriptome of IM at steady-state and IM 1 week after administration of 50 Âµg CpG-DNA intratracheally.

2017-03-01 | E-MTAB-5012 | biostudies-arrayexpress

Transcriptome analysis of pulmonary CCR2+ inflammatory monocytes challenged with Cryptococcus neoformans

Project description:The encapsulated yeast Cryptococcus neoformans can cause a fatal meningoencephalitis in immunocompromised patients. C. neoformans infection is acquired through the respiratory tract, but the cellular and molecular mechanisms of the pulmonary innate immune response are still not well defined. To investigate the response of CCR2+ inflammatory monocytes to C. neoformans, we compared the transcriptomes of CCR2+ inflammatory monocytes from the lungs of naïve versus infected mice.

2019-02-11 | GSE122765 | GEO

Gene expression profiles of mouse monocytes deficient in the CCL2/CCR2 chemokine signaling

Project description:Gene-level transcriptome analysis of monocyte mRNA derived from mice that are genetically deficient of the Ccl2 gene or Ccr2 gene The CCL2/CCR2 chemokine axis is critical in monocytes mobilization and innate immunity. Although mice deficient in either gene manifest similar phenotype, such as reduced atherosclerosis, some biologic processes are disrupted in starkly different ways in these mice. We found in a Her2/neu driven mammary carcinoma model, the absence of Ccl2 inhibits tumor growth and prolongs survival, while genetic deletion of Ccr2 has the opposite effect. One of the postulated mechanisms is that Ccl2 and Ccr2 affect monocyte development in different manners. This experiment was designed to compare the whole transcriptome of monocytes that are deficient in either Ccl2 or Ccr2, with the hypothesis that differential development of these monocytes will manifest as differential gene expression profiles.

2016-10-21 | GSE88962 | GEO

Tumor-infiltrating CCR2+ inflammatory monocytes counteract specific immunotherapy

Project description:Tumor-infiltrating CCR2+ inflammatory monocytes counteract specific immunotherapy

| PRJNA1001913 | ENA