ECCM treated BMDC
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
SUBMITTER: Michael Weitnauer
PROVIDER: E-MTAB-2517 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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2013-09-17 | E-GEOD-50898 | biostudies-arrayexpress
Project description:Microbial molecules have evolved to promote transient and/or permanent associations with mammals. Although numerous examples of secretion systems employed by pathogens have been described, mechanisms by which commensal bacteria export molecules during symbiosis remain unknown. The human gut mutualist Bacteroides fragilis produces a capsular polysaccharide (PSA) that directs host immune development. We reveal herein that outer membrane vesicles (OMVs) deliver PSA to dendritic cells (DCs), promoting regulatory T cells and inducing anti-inflammatory cytokines during protection from intestinal disease. In addition, we found that TLR2 signaling by DCs is required for OMV sensing. Following internalization into DCs and engagement of TLR2, OMVs initiate a gene expression program that results in IL-10 production by DCs. Although it is known that the outcome of PSA sensing by the immune system is Treg induction, nothing is known about the intracellular signaling pathway(s) activated by PSA within DCs. We analyzed the gene expression profile of DCs treated with OMVs to uncover factors that are expressed in a PSA-dependent, TLR2-dependent manner. Our findings demonstrate DC-induced protection from disease via OMV-delivery of a beneficial microbial molecule, uncovering a novel paradigm for inter-kingdom communication between the microbiota and mammals. RNA samples (1ug total RNA) from BMDCs were labeled with fluorescent dyes using the Quick Amp Labeling Kit (Agilent). Microarray (AgilentWhole Mouse Genome chip) hybridizations (65M-BM-0C for 16 hours) and washes were performed with Agilent reagents following standard protocols. Microarrays were analyzed using an Agilent DNA Microarray Scanner G2565CA, and data were acquired using Agilent's Feature Extraction Software version 10.1.1.1. Significant genes were selected based on p< 0.01 and fold change >2.0.
2012-07-22 | E-GEOD-39563 | biostudies-arrayexpress
Project description:Dendritic cells (DCs) are the most potent antigen (Ag)-presenting cells. Whereas immature DCs down-regulate T cell responses to induce/maintain immunological tolerance, mature DCs promote immunity. To amplify their functions, DCs communicate with neighboring DCs through soluble mediators, cell-to-cell contact and vesicle exchange. Transfer of nanovesicles (<100nm) derived from the endocytic pathway (termed exosomes) represents a novel mechanism of DC-to-DC communication. The facts that exosomes contain exosome-shuttle microRNAs (miRNAs), and DC functions can be regulated by exogenous miRNAs, suggest that DC-to-DC interactions could be mediated through exosome-shuttle miRNAs, an hypothesis that remains to be tested. Importantly, the mechanism of transfer of exosome-shuttle miRNAs from the exosome lumen to the cytosol of target cells is unknown. Here, we demonstrate that DCs release exosomes with different miRNAs depending on the maturation of the DCs. By visualizing spontaneous transfer of exosomes between DCs, we demonstrate that exosomes fused with the target DCs, the latter followed by release of the exosome content into the DC cytosol. Importantly, exosome-shuttle miRNAs are functional, as they repress target mRNAs of acceptor DCs. Our findings unveil a mechanism of transfer of exosome-shuttle miRNAs between DCs and its role as a means of communication and post-transcriptional regulation between DCs. The study has analyzed the microRNA content of 4 samples of immature exosomes, 4 samples of matures exosomes, 2 samples of immature bone-marrow-derived DCs, and 2 samples of mature bone marrow-derived DCs.
2011-10-24 | E-GEOD-33179 | biostudies-arrayexpress
Project description:Fibroblasts usually mediate acute wound healing and long-term tissue remodeling with scarring in tissue injury. In myocardial infarction (MI), following a prolonged lack of oxygen supply, necrotized cardiomyocytes become replaced by secreted extracellular matrix proteins produced by fibroblasts. Dendritic cells (DCs) act as inflammatory cells and can migrate from the bone marrow to the infarct areas and infarct border areas to mediate collagen accumulation after MI, whereas trichostatin A (TSA) can regulate the apoptosis and proliferation of the fibroblasts and affect DCs functions under oxygen–glucose deprivation (OGD) conditions. In this study, we used proteomics to investigate the effects of TSA and bone marrow-derived dendritic cells (BMDCs) on NIH3T3 fibroblasts under OGD conditions. Results showed that the fatty acid degradation pathway was significantly upregulated in NIH3T3 cells under OGD conditions, and the fatty acid synthesis pathway was significantly downregulated in NIH3T3 cells treated with BMDCs conditioned media with TSA (BMDCs-CM[TSA]) under OGD conditions. Meanwhile, the BMDCs-CM(TSA) significantly decreased the levels of triglycerides and free fatty acids and mediated ten fatty acid metabolism-related proteins in the NIH3T3 cells under OGD conditions. Summarily, the proteomic analysis showed that TSA and BMDCs affect fatty acid metabolism in NIH3T3 cells under OGD conditions.
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Project description:The aim of this study was to analyze expression differences between murine splenic miR-146a deficient and miR-146a sufficient T cells after allogeneic stimulation in vitro.
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Project description:Dendritic cells isolated from murine bone marrow were cultured for 7 days and then stimulated with 100 ng/mL LPS for 24h. Cells were derived from either wildtype or microRNA-146a knock-out mice. Total RNA was isolated from the cells following stimulation.
2016-07-30 | E-MTAB-3539 | biostudies-arrayexpress
Project description:The Suppressor of cytokine signaling (SOCS) family of negative regulatory proteins are upregulated in response to several cytokines and pathogen-associated molecular patterns (PAMPs), and suppress cellular signaling responses by binding receptor phosphotyrosine residues. Exposure of bone marrow-derived dendritic cells (BMDCs) to 1D8 cells, a murine model of ovarian carcinoma, suppresses their ability to express CD40 and stimulate antigen specific responses in response to PAMPs, and in particular to poly I: C with the upregulated SOCS3 transcript and protein levels. The ectopic expression of SOCS3 in both the macrophage cell line RAW264.7 and BMDCs decreased signaling in response to both poly I:C and IFNα. Further, knockdown of SOCS3 transcripts significantly enhanced the responses of RAW264.7 and BMDCs to both poly I: C and IFNα. Immunoprecipitation and pull-down studies demonstrate that SOCS3 binds to the IFNα receptor TYK2. Since poly I: C triggers autocrine IFNα signaling, binding of SOCS3 to TYK2 may thereby suppress the activation of BMDCs by polyI:C and IFNα. Thus, elevated levels of SOCS3 in tumor-associated DCs may potentially resist the signals induced by TLR3 ligands and type I interferon to decrease DC activation via binding with IFNα receptor TyK2. Experiment Overall Design: Microarray analysis was used to compare the expression levels of Control mouse bone marrow-derived dendritic cells (BMDC), with cells that had been cocultured (1:5, tumor:BMDC) with mouse ovarian surface epithelial cell line (1D8) cells, with irradiated (50Gy) 1D8 cells, or with the supernatent from 1D8 cells (25%, v/v). Experiment Overall Design: One biologic sample was analyzed for each condition, four samples in all.
2009-02-28 | E-GEOD-10741 | biostudies-arrayexpress
Project description:Endogenous damage associated molecular pattern molecules (DAMPs) released from necrotic, damaged or stressed cells are associated with an inflammatory response. Whether the microRNA expression signature of this response is different from that of a PAMP-stimulated inflammatory response is unknown. We report here that miR-34c and miR-214 are significantly expressed in fresh human PBMCs exposed to DAMPcontaining freeze-thaw lysates, or to conditioned media from serum-starved and glucose-deprived cells (p<6x10-4 and p<3.7x10-3), respectively. Interestingly, only miR-34c expression was differentially expressed in PBMCs exposed to freeze-thaw lysates or conditioned media from HMGB1+/+ mouse embryonic fibroblast (MEF) cells, when compared to cultures exposed to lysates or conditioned media from HMGB1-/- MEFs. miR-155 expression in these cultures was negligible, but was significantly higher in PBMCs stimulated with LPS or most other TLR ligands, making it the prototypic PAMPmiR. Exposure to a damaged human colorectal carcinoma cell line lysate (HCT116) similarly resulted in increased miR-34c and miR-214 levels. When PBMCs were pre-transfected with anti-miR-34c and then exposed to lysate, expression levels of IKKgamma mRNA, a putative target of miR-34c, increased, while protein levels of IKKgamma in cultures transfected with a pre-miR-34c were abrogated. Levels of miR-34c expression (as well as pro-inflammatory cytokines, IL-1beta and TNFalpha) decreased when PBMC cultures were briefly pre-incubated with the K+ channel (inflammasome) inhibitor, glybenclamide, suggesting that miR-34c is involved in the inflammasome pathway in response to DAMPs. Our findings suggest that a specific microRNA expression signature is associated with the inflammatory response to damaged/injured cells and carries implications for many acute and chronic inflammatory disorders. Human PBMC (peripheral blood mononuclear cells) were exposed to 4 conditions for 48 hours. In the first condition, PBMCs were exposed to conditioned media from serum-starved and glucose-deprived and heat shocked HMGB1-/- MEF cells (mouse embryonic fibroblast cells). In the second condition, PBMCs were exposed to conditioned media from serum-starved and glucose-deprived and heat shocked HMGB1+/+ MEF cells (mouse embryonic fibroblast cells). In the third condition, PBMCs were exposed to LPS (Lipopolysaccharide). In the fourth condition, the PBMCs where left untreated. Four biological repeats were done for each condition for a total of 16 samples.
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