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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Global gene expression changes during immune complex-induced neutrophil activation (wild type and Card9â??/â?? cells)

ABSTRACT: --- Raw data of the Supplementary Table 1 of the Nature Communications article 'Neutrophil-specific deletion of the CARD9 gene expression regulator suppresses autoantibody-induced inflammation in vivo' We used microarray to obtain global gene expression data of immobilised immune complex-activated mouse neutrophils in the presence and absence of the gene expression regulator molecule CARD9. Mouse neutrophils were isolated from the bone marrow and were plated on human serum albumin & anti-human serum albumin antibody-coated surfaces at a 4 x 106 cell concentration. Human serum albumin-coated surfaces served as controls. The cells were stimulated for 4 hours before RNA preparation. The experiments were done at 3 independent timepoints.

ORGANISM(S): Mus musculus

SUBMITTER: Attila Mocsai

PROVIDER: E-GEOD-78066 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Global gene expression changes during immune complex-induced neutrophil activation (wild type and Card9‒/‒ cells)

Project description:--- Raw data of the Supplementary Table 1 of the Nature Communications article 'Neutrophil-specific deletion of the CARD9 gene expression regulator suppresses autoantibody-induced inflammation in vivo' We used microarray to obtain global gene expression data of immobilised immune complex-activated mouse neutrophils in the presence and absence of the gene expression regulator molecule CARD9.

2016-02-29 | GSE78066 | GEO

Genome-wide analysis of the CARD9/Dectin-1 transcriptional program in neutrophils and macrophages by RNA-seq

Project description:Purpose: To characterize Card9-dependent and Card9-independent Dectin-1 mediated gene expression changes in neutrophils and to compare response to Dectin-1 stimulation in neutrophils and macrophages. Method: BM neutrophils from WT and Card9-/- mice were isolated by MACS column purification and treated with or without the Dectin-1 agonist, curdlan for 3 hrs. WT BM-derived macrophages were also treated with or without curdlan for 3hrs before sample collection. Results: We identified both Card9-dependent and Card9-independent gene expression changes with Dectin-1 stimulation in neutrophils. We also identified cell-type specific differences in the response to Dectin-1 stimulation in neutrophils and macrophages. Conclusions: Dectin-1 stimulation induces significant gene expression changes regulated by either canonical Card9-dependent or non-canonical Card9-independent mechanisms.

2021-02-26 | GSE148850 | GEO

E-MTAB-7212

Project description:Investigation of titanium coated imprinted polystyrene surfaces

2019-02-11 | E-MTAB-7212 | ExpressionAtlas

Investigation of titanium coated imprinted polystyrene surfaces

Project description:In this study the gene expression differences between two titanium surfaces produced at Maastricht University were investigated. These two surfaces were: flat titanium-coated polystyrene and a titanium-coated polystyrene surface imprinted with a pattern selected from an earlier screening study (Ti1018). This pattern was selected based on the osteoinductive properties observed. As a positive control cells on the flat surface were treated with dexamethasone.

2018-09-25 | E-MTAB-7212 | biostudies-arrayexpress

Transcriptomic fingerprints of C. elegans exposed to superparamagnetic iron oxide nanoparticles coated with a monolayer of bovine serum albumin (BSA-SPIONs)

Project description:Superparamagnetic Iron Oxide Nanoparticles (SPIONs) are currently being investigated for a range of biomedical applications. Their use have been related with different cytotoxic mechanisms including the generation of oxidative stress and the induction of metal detoxification pathways, among others. Different NP coatings are being explored, among them albumin which has been applied in some drugs delivery systems. We have investigated the molecular mechanisms responsive to in-house fabricated SPIONs coated with bovine serum albumin (BSA-SPIONs) in the nematode C. elegans to compare in vivo findings with previous in vitro studies. BSA-SPIONs (500 µg/ml) affected the transcriptional response of glycan metabolic pathways related to innate immune response, xenobiotics degradation, and triggered a lysosomal response, indicating a relevant biological role of this cellular compartment in the response to this nanoparticle treatment in C. elegans. Remarkably, key biological functions such as apoptosis or protein processing were not affected with significance despite the high dose of exposure.

2018-01-05 | GSE93186 | GEO

Project description:Effect of Human serum albumin on Acinetobacter baumannii

| PRJNA474613 | ENA

Differential gene expression between Salmonella Typhimurium biofilms on glass vs cholesterol surfaces

Project description:Salmonella spp. biofilms have been implicated in persistence in the environment and plant surfaces. In addition, Salmonella is able to form biofilms on the surface on cholesterol gallstones. The ability of Salmonella spp. on these surfaces is superior to biofilm formation on surfaces on glass or plastic. Thus, we hypothesized that Salmonella gene expression is specific during biofilm development on cholesterol surfaces. Flow through assays were performed whereby S. Typhimurium was inoculated into chambers coated with glass or cholesterol. At 24h post-inoculation, planktonic (from the flow through), biofilms (from glass or cholesterol) were collected. Thus we had 4 samples: Planktonic (2) and Biofilms (2), each with 2 biological replicates

2013-07-09 | E-GEOD-48604 | biostudies-arrayexpress

Colon gene expression signatures in wild type and Card9-/-mice exposed to DSS induced colitis

Project description:It is crucial to decipher the host-microbiota interactions as they are involved in intestinal homeostasis and diseases. Caspase Recruitment Domain 9 (Card9) is an inflammatory bowel disease (IBD) susceptibility gene coding for an adapter protein for innate immunity toward many microorganisms. Card9 mediates colitis recovery via interleukin 22 pathway activation and Card9-/- mice have enhanced susceptibility to colitis. To reveal the mechanisms responsible of this defect in Card9-/-mice, we compared colon transcriptomics in WT and Card9-/- mice before and during DSS-induced colitis. Mice transcriptomes clusterized according to the genotype supporting a pattern clearly different in WT and Card9-/- mice. The number of up-regulated genes at day 7 was largely higher in Card9-/- compared to WT mice. Pathway analyses of the induced transcripts showed a dominance of immune-related pathway with a stronger signal in Card9-/- mice. Interestingly, NOD-like receptor signaling pathway, in which CARD9 is involved, was an exception with weaker activation in Card9-/- than in WT mice. During the recovery period at day 12, pathways involved in cell proliferation and replication were significantly activated in WT compared to Card9-/- mice confirming the healing defect in Card9-/- mice. For the induction of colitis, mice were given drinking water supplemented with 2% (w/v) Dextran sulphate sodium (DSS) for 7 days, then allowed to recover by drinking water alone for 5 additional days. 3 mice of each groups (WT and Card9-/-) were sacrified before DSS administration. 5 WT mice and 4 Card9-/- mice were sacrified 7 days after DSS administration and 5 mice of each group were sacrified at day 12.

2016-04-05 | E-GEOD-67577 | biostudies-arrayexpress

Caenorhabditis elegans

Project description:Transcriptomic fingerprints of C. elegans exposed to superparamagnetic iron oxide nanoparticles coated with a monolayer of bovine serum albumin (BSA-SPIONs)

| PRJNA360346 | ENA

Card9 protects zymosan-induced peritonitis through regulating autophagy in macrophage

Project description:CARD9 is an adapter protein, which plays a critical role in anti-fungal immunity. However, the role of CARD9 in fungal-induced autophagy remains unknown. In this study, we demonstrated that Card9-/- mice displayed more severe phenotype of zymosan-induced peritonitis, presenting as multiple organs injury and increased systemic inflammation. Moreover, the number of macrophage in spleen was increased in Card9-/- mice. Further studies revealed that autophagy was impaired in peritoneal macrophages of Card9-/- -peritonitis mice. Notably, the autophagy agonist, rapamycin, ameliorated peritonitis in Card9-/- mice. Moreover, Card9 mediates the interaction of Malt1 and P62 upon zymosan stimulation. Together, our results confirmed the protective role of Card9 in the development of peritonitis via regulates autophagy in macrophage cells. The study indicates Card9 may be a potential therapeutic target for peritonitis.

2024-01-01 | GSE164572 | GEO

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