Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

59 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcription profiling of human monocytes and monocyte-derived macrophages infected with Coxiella burnetii and incubated with apoptotic or necrotic lymphocytes

ABSTRACT: Q fever is due to Coxiella burnetii, an obligate intracellular bacterium. We investigated the mechanism of establishment of chronic form of the Q fever that mainlym anifested by endocarditis. We showed that patients with acute Q fever and valvulopathy, who have the higher risk to develop an endocarditis, exhibited high levels of circulating apoptotic cells. We further investigated the effect of the uptake of dead cells on the intracellular fate of the bacterium and the immune response of monocytes and macrophages.

INSTRUMENT(S): other

ORGANISM(S): Homo sapiens

DISEASE(S): C. burnetii infected

SUBMITTER: Marie Benoit

PROVIDER: E-MEXP-1289 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Orientia tsutsugamushi, the agent of scrub typhus, induces an inflammatory program in human macrophages

Project description:Scrub typhus is a life-threatening disease caused by Orientia tsutsugamushi, a bacterium that mainly infects endothelial cells in vitro and in vivo. Evidence suggests that the interaction of O. tsutsugamushi with myeloid cells may play a pivotal role in O. tsutsugamushi infection. We showed here that O. tsutsugamushi intensively replicated within human monocyte-derived macrophages. Bacterial organisms stimulated the expression of a large panel of genes including type I interferon, interferon-stimulated, inflammatory, apoptosis-related genes and induced an M1-type gene response in macrophages. This transcriptional signature was accompanied by functional consequences such as the release of inflammatory cytokines such as Tumor Necrosis Factor and interleukin-gamma. Live O. tsutsugamushi organisms were necessary for type I interferon response and, to a lesser degree, to inflammatory response. As interferon-gamma is known to elicit M1 polarization, we assessed the effect of interferon-gamma on O. tsutsugamushi fate in macrophages. Exogenous interferon-gamma partly inhibited O. tsutsugamushi replication within macrophages. Our results suggest that the inflammatory response induced by O. tsutsugamushi may account for the local and systemic inflammation observed in scrub typhus and that interferon-gamma may be useful as an adjuvant treatment of patients with scrub typhus. Macrophages (4 M-CM-^W 10.5 cells per assay) were incubated with O. tsutsugamushi at a bacterium-to-cell ratio of 20:1 for 8 hours. RNA samples (four samples per experimental condition) were processed for microarray analysis.

2013-01-29 | E-GEOD-38194 | biostudies-arrayexpress

Granulomatous response to Coxiella burnetii, the agent of Q fever: Activation of type I interferon-related genes

Project description:The formation of granulomas is associated with the resolution of Q fever, a zoonosis due to Coxiella burnetii; however the molecular mechanisms of granuloma formation remain poorly understood. We generated human granulomas with peripheral blood mononuclear cells and beads coated with C. burnetii, using BCG extracts as controls. A microarray analysis showed dramatic changes in gene expression in granuloma cells compared with peripheral blood mononuclear cells. About 60% of modulated genes were common to C. burnetii and BCG granulomas including M1-related genes. C. burnetii granulomas also expressed a specific transcriptional profile that was essentially enriched in genes associated with type I interferon response (IFI44, IFI44L, IFI6, OAS1, OAS2, OAS3, ISG15, IFIT1, IFITM2, IFITM3, MX1 and MX2). Real-time RT-PCR confirmed that C. burnetii especially increased the expression of interferon-stimulated genes in granulomas generated from controls or Q fever patients. Our results showed that granuloma formation is associated with a core of transcriptional response, but that the granulomatous response to C. burnetii is characterized by the activation of type I interferon-related genes, conferring a new role for type I interferon response in the control of C. burnetii infection. Human Peripheral Blood Mononuclear Cells (PBMC) were co-cultured with beads coated with Mycobacterium bovis strain Bacille Calmette Guerin (BCG) extracts or Coxiella burnetii (C.burnetii) extracts for 8 days and PBMC at day 0 were used as controls. For each condition ( unstimulated, BCG and C.burnetii), each microarray is a replicate of the same biological sample.

2015-05-01 | E-GEOD-37666 | biostudies-arrayexpress

Discovery of a druggable copper-signaling pathway that drives inflammation

Project description:Quantitative mass-spectrometry-based proteomics in MDM during inflammation.

2023-04-06 | PXD038612 | Pride

The Paradigm of Macrophage Polarization is not Applicable per seto Human Circulating Monocytes

Project description:Macrophage activation is required for the control of innate and adaptive immune responses. The classification in M1 and M2 macrophages based on a combination of small numbers of membrane and soluble markers is operational in murine and human macrophages. If this classification may be extended to circulating monocytes is not elucidated. To answer such question, human monocytes were stimulated for 6 and 18 hours with IFN-gamma and IL-4, two canonical agonists of M1/M2 polarization in macrophages, and gene expression programs were investigated with whole genome microarrays. The temporal analysis of these programs showed marked differences to both IFN-gamma and IL-4. In 6-h stimulated monocytes, gene categories related to inflammatory and immune responses were enriched, and these monocytes exhibited a M1 and M2 polarization in response to IFN-gamma and IL-4, respectively, as found in macrophages. In 18-h stimulated monocytes, the categories related to innate immunity and metabolic pathways were enriched in response to IFN-gamma and IL-4, whereas PPAR signaling pathway was specifically enriched in response to IL-4. In addition, the M1 and M2 polarization induced by IFN-gamma and IL-4, respectively, was replaced by an original transcriptional program that did not depend on IFN-gamma and IL-4. This program appeared as networks around chemokines, NF-kappaB/MAP kinase pathways and MHC class II molecules. These results clearly demonstrated that monocyte activation consisted of an early polarized stage likely involved in effector responses and a delayed stage that may regulate host responses. The establishment of databases on human circulating monocytes using high throughput methods may be critical for pathophysiological and clinical non-invasive studies. Peripheral blood mononuclear cells (PBMCs) were isolated from leukopacks from normal blood donor buffy coats (Etablissement FranÃ§ais du Sang, Marseille, France) by Ficoll density gradient

2012-12-07 | E-GEOD-27658 | biostudies-arrayexpress

RNA-seq of primary human monocytes (4 healthy donors)

Project description:Monocytes were isolated from healthy donors PBMC and sorted for classical and non-classical monocyte subsets. RNA-seq was performed on unstimulated monocytes.

2018-11-09 | E-MTAB-6712 | biostudies-arrayexpress

The proteome of neutrophils in sickle cell disease

Project description:Polymorphonuclear neutrophils are key actors in the pathophysiology of sickle cell disease, but specific factors underlying their activation and sustained inflammation are not well documented. In the present study, we investigated the proteome of neutrophils by a label-free global comparative approach between 4 non-treated sickle patients (SS genotype) at steady state and 4 healthy donors. We identified 101 proteins differentially expressed in SS and normal neutrophils. We found overexpression of CD64 and under-expression of CD62L suggestive of an activated and aged neutrophil profile in SS patients. Comparison of the two proteomes revealed a strong involvement of the type 1 interferon (IFN) response pathway with a 3- to 84-fold increase of type 1 IFN-induced proteins in SS neutrophils, and overexpression of STAT1 and STAT2. Thus, we next determined the plasmatic concentration of type 1 IFNs (IFNα and IFNβ) using the digital-ELISA technology and found a significant higher concentration of IFNα in the plasma from half of our SS patients compared to controls. Overall, a dramatic high-level expression of IFNα signaling proteins in neutrophils from SS patients suggests auto-inflammatory-like phenotype in sickle cell disease at steady state. This finding could open the way to new anti-inflammatory therapies.

2020-11-11 | PXD014457 | Pride

ChIP-seq of EGR1 in human primary unstimulated monocytes and in unstimulated human monocytes from three CMML patients

Project description:Identification of EGR1 chromatin localization in human primary monocytes (2 donors), in human primary monocytes from 2 CMML patients with TET2 truncating mutations (high VAF) and in human primary monocytes from 1 CMML patients with TET2 truncating mutations with low VAF.

2021-11-15 | E-MTAB-11132 | biostudies-arrayexpress

ChiP-seq of H3K4me3 in primary unstimulated monocytes from 3 healthy donors buffy coats and from 4 CMML patients

Project description:Identification of H3K4me3 localization on chromatin in primary unstimulated monocytes

2018-11-09 | E-MTAB-6689 | biostudies-arrayexpress

Project description:Background: Hepatitis E Virus (HEV) is a new causative agent of chronic hepatitis in solid organ transplant recipients in Europe. Factors associated with the occurrence and persistence of chronic HEV infection remain largely unknown but chronic evolution seems to be the consequence of hostM-bM-^@M-^Ys immunological factors rather than of viral factors. Method: In a prospective case-control study, we have determined in whole blood of chronically HEV-infected kidney-transplant recipients the host response using microarray technology. Results: Chronically HEV-infected kidney-transplant recipients exhibited a specific transcriptional program, in which interferon effectors were prominent. The intensity of expression of each signatureM-bM-^@M-^Ys gene was significantly lower in patients who were subsequently cleared of HEV than in patients who were not. Furthermore, in patients who were cleared of HEV, a higher expression of these genes was associated with a longer delay until HEV clearance. Conclusions: The specific transcriptional program determined in chronically HEV-infected kidney-transplant recipients suggests an activation of type I interferon response. Intensity of interferon-stimulated genes expression could be useful to forecast the outcome of infection. High expression of interferon-stimulated genes could signify a dysregulation in the interferon response that might favour the persistence of the HEV infection. TrialM-bM-^@M-^Ys registration number: NCT01090232; RegistryM-bM-^@M-^Ys URL: http://clinicaltrials.gov/ct2/show/study/NCT01090232?term=kidney+transplant+recipients&cntry1=EU%3AFR&rank=2 Total RNA was extracted from whole-blood sample or monocytes of kidney-transplant patients with or without chronic hepatitis E (CHE) infection. Control patients were matched up with CHE patients for age, sex, time since kidney transplant and immunosuppressive treatment.

2013-01-29 | E-GEOD-36539 | biostudies-arrayexpress

Gene expression profiling of naive B cells

Project description:Whole genome gene expression microarrays made it possible to pick up genes, whose products could be involved in a biological pathway. The aim of this study is to provide easy tools to interrogate whole genome transcriptome changes in the process of plasma cell generation, starting from naive B cells and comprising centroblasts, centrocytes, memory B cells, preplasmablasts, plasmablasts, early plasma cells, and mature bone marrow plasma cells.

2013-07-10 | E-MTAB-1771 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data