Transcriptome analysis of pulmonary CCR2+ inflammatory monocytes challenged with Cryptococcus neoformans
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA506250 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR8217100_1.fastq.gz | Fastqsanger.gz | |||
| SRR8217100_2.fastq.gz | Fastqsanger.gz | |||
| SRR8217101_1.fastq.gz | Fastqsanger.gz | |||
| SRR8217101_2.fastq.gz | Fastqsanger.gz | |||
| SRR8217102_1.fastq.gz | Fastqsanger.gz |
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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.
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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
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.
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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.
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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.
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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.
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Project description:Comparative analysis of FACS-sorted CCR2- and CCR2+ HSC in the steady state. CCR2+ HSC have fourfold higher proliferative rates than CCR2- HSC, are are biased towards the myeloid lineage and dominate the migratory HSC population. Comparison of pooled CCR2- and CCR2+ HSC (bone marrow from 20 mice pooled for each sample), three biological replicates each.
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Project description:The interactions between chemokines and their receptors, particularly in the context of inflammation, are complex with individual receptors binding multiple ligands and individual ligands interacting with multiple receptors. In addition, there are numerous reports of simultaneous co-expression of multiple inflammatory chemokine receptors on individual inflammatory leukocyte subtypes. Overall, this has previously been interpreted as redundancy and proposed as a protective mechanism to ensure that the inflammatory response is robust. In contrast we have hypothesised that the system is not redundant but exquisitely subtle. Our interests relate to the receptors CCR1, CCR2, CCR3 and CCR5 which, together, regulate non-neutrophilic myeloid cell recruitment to inflammatory sites. Here we demonstrate that, whilst most murine monocytes exclusively express CCR2, there is a small subpopulation, which is expanded during inflammation, which co-expresses CCR1 and CCR2. Combinations of transcript and functional analysis demonstrate that this is not redundant expression and that co-expression of CCR1 and CCR2 marks a phenotypically distinct population of monocytes characterised by expression of genes otherwise typically associated with neutrophils. Single cell RNA sequencing confirms this as a monodisperse population of atypical monocytes. This monocytic population has been previously described as having immunosuppressive activity. Overall, our data confirm combinatorial chemokine receptor expression by a subpopulation of monocytes but demonstrate that this is not redundant expression and marks a discrete monocytic population.
2024-07-10 | GSE251646 | GEO
Project description:The interactions between chemokines and their receptors, particularly in the context of inflammation, are complex with individual receptors binding multiple ligands and individual ligands interacting with multiple receptors. In addition, there are numerous reports of simultaneous co-expression of multiple inflammatory chemokine receptors on individual inflammatory leukocyte subtypes. Overall, this has previously been interpreted as redundancy and proposed as a protective mechanism to ensure that the inflammatory response is robust. In contrast we have hypothesised that the system is not redundant but exquisitely subtle. Our interests relate to the receptors CCR1, CCR2, CCR3 and CCR5 which, together, regulate non-neutrophilic myeloid cell recruitment to inflammatory sites. Here we demonstrate that, whilst most murine monocytes exclusively express CCR2, there is a small subpopulation, which is expanded during inflammation, which co-expresses CCR1 and CCR2. Combinations of transcript and functional analysis demonstrate that this is not redundant expression and that co-expression of CCR1 and CCR2 marks a phenotypically distinct population of monocytes characterised by expression of genes otherwise typically associated with neutrophils. Single cell RNA sequencing confirms this as a monodisperse population of atypical monocytes. This monocytic population has been previously described as having immunosuppressive activity. Overall, our data confirm combinatorial chemokine receptor expression by a subpopulation of monocytes but demonstrate that this is not redundant expression and marks a discrete monocytic population.
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Project description:Leukocyte recruitment, a universal feature of tissue inflammation, is regulated by the interactions of chemokines with their G protein-coupled receptors. Activation of CC chemokine receptor 2 (CCR2) by its cognate chemokine ligands, including CCL2, plays a central role in recruitment of monocytes in several inflammatory diseases. In this study, we used phosphoproteomics to enable unbiased characterization of the signaling network resulting from CCL2 activation of CCR2. Using data-independent acquisition (DIA) mass spectrometry, both the proteome and phosphoproteome were quantified for FlpIn-HEK293T cells stably expressing CCR2, at six time points after activation with CCL2, in comparison with untreated cells. Differential expression analysis identified 699 significantly regulated phosphorylation sites located on 441 proteins. As expected, many of these proteins participate in canonical signal transduction pathways and the regulation of actin cytoskeleton dynamics, including numerous guanine nucleotide exchange factors (GEFs) and GTPase activating proteins (GAPs). In addition, we identified regulated phosphorylation sites in numerous proteins that exert functions in the nucleus, including several constituents of the nuclear pore complex. This study provides an unprecedented level of detail about CCR2 signalling and identifies potential novel targets for regulation of CCR2 function.
2020-04-08 | PXD015845 | Pride