Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA114787 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Time-course of gene expression in BMDCs stimulated with gamma-PGA nanoparticles
| PRJNA114791 | ENA
Project description:The gene expression levels in murine bone marrow-derived dendritic cells treated with γ-PGA NPs were examined by oligonucleitide microarray and compared with those in the cells treated with other adjuvants. The gene expression of proinflammatory chemokines, cytokines, and costimulatory molecules was upregulated considerably in DCs treated with γ-PGA NPs. The upregulation pattern was similar to that in DCs treated with LPS but not in DCs treated with unparticulate γ-PGA. The activation of DCs by γ-PGA NPs was confirmed by real-time RT-PCR analysis for the genes related to TLR signaling. The effect of γ-PGA NPs on DCs was not annihilated by treating with polymixin B, an inhibitor of LPS. Furthermore, the immunization of mice with γ-PGA NPs carrying OVA significantly induced Ag-specific CD8+ T cells and Ag-specific production of IL-2, TNF-α, and IFN-γ from the cells. Such activities of γ-PGA NPs were more prominent, when compared to the immunization with OVA plus aluminum hydroxide or OVA plus CFA. These results suggest that γ-PGA NPs induce a CD8+ T cell response through activating innate immunity in a fashion different from that of LPS. Thus, γ-PGA NPs may be an attractive adjuvant to be further developed for vaccine therapy.
2009-03-05 | GSE15087 | GEO
Project description:Nitidine Chloride(NC) were found to enhance IL-10 production in LPS-stimulated Bone-marrow dendritic cells(BMDCs ) ,while at the same time inhibit pro-inflammatory cytokines production, such as TNF- α and IL-6. BMDCs were treated with NC or vehicle following LPS stimulation to find out the influence of NC on BMDCs that regulate cytokines expression. This study indicated that NC regulate numerous gene expression, thus influence IL-10 and pro-inflammatory cytokines production in LPS-treated BMDCs.
2017-08-05 | GSE102135 | GEO
Project description:This is an investigation of whole genome gene expression level in tissues of mice stimulated by LPS, FK565 or LPS + FK565 in vivo and ex vivo. We show that parenteral administration of a pure synthetic Nod1 ligand, FK565, induces site-specific vascular inflammation in mice, which is prominent in aortic root including aortic valves, slight in aorta and absent in other arteries. The degree of respective vascular inflammation is associated with persistent high expression of proinflammatory chemokine/cytokine genes in each tissue in vivo by microarray analysis, and not with Nod1 expression levels. The ex vivo production of proinflammatory chemokine/cytokine by Nod1 ligand is higher in aortic root than in other arteries from normal murine vascular tissues, and also higher in human coronary artery endothelial cells (HCAEC) than in human pulmonary artery endothelial cells (HPAEC), suggesting that site-specific vascular inflammation is at least in part ascribed to an intrinsic nature of the vascular tissue/cell itself. A fourty chip study using total RNA recovered from four isolated tissues of mice which were stimulated by various reagents. Aortic root, pulmonary artery, aorta and spleen of mice in 3 groups: 1) intraperitoneal injection of 20M-NM-<g of LPS priming only, 2) oral administration of FK565 (100M-NM-<g) for consecutive days, 3) oral administration of FK565 (100M-NM-<g) for consecutive days 1 day after LPS priming, at day 2, 4, and 7. And six chip study using total RNA recovered from three isolated vascular tissues of mice which were stimulated by FK565 (10M-NM-<g/mL) ex vivo.
2011-03-01 | E-GEOD-20930 | biostudies-arrayexpress
Project description:This is an investigation of whole genome gene expression level in tissues of mice stimulated by LPS, FK565 or LPS + FK565 in vivo and ex vivo. We show that parenteral administration of a pure synthetic Nod1 ligand, FK565, induces site-specific vascular inflammation in mice, which is prominent in aortic root including aortic valves, slight in aorta and absent in other arteries. The degree of respective vascular inflammation is associated with persistent high expression of proinflammatory chemokine/cytokine genes in each tissue in vivo by microarray analysis, and not with Nod1 expression levels. The ex vivo production of proinflammatory chemokine/cytokine by Nod1 ligand is higher in aortic root than in other arteries from normal murine vascular tissues, and also higher in human coronary artery endothelial cells (HCAEC) than in human pulmonary artery endothelial cells (HPAEC), suggesting that site-specific vascular inflammation is at least in part ascribed to an intrinsic nature of the vascular tissue/cell itself.
2011-03-01 | GSE20930 | GEO
Project description: Not available
| S-EPMC8784167 | biostudies-literature
Project description:Expression data from BMDCs treated with BI2536 or vehicle control and stimulated with LPS or poly(I:C)
| PRJNA138967 | ENA
Project description:The gene expression levels in murine bone marrow-derived dendritic cells treated with γ-PGA NPs were examined by oligonucleitide microarray at 6, 12 and 24 hours. The gene expression of proinflammatory chemokines, cytokines, and costimulatory molecules was upregulated considerably in DCs treated with γ-PGA NPs at 6 hours.
2009-03-05 | GSE15089 | GEO
Project description:We used microarrays to detail the global programme of gene expression underlying Polo-like kinase inhibition with BI 2536 compound in mouse bone marrow-derived dendritic cells (BMDCs) stimulated with Toll-like receptor agonists LPS and poly(I:C). CD11c+ BMDCs were treated for 1 hour with BI 2536 (1µM) or vehicle control (DMSO) prior to stimulation with LPS or poly(I:C) for 4 h. Total RNA was extracted and prepared for hybridization on Affymetrix microarrays.
2011-04-12 | E-GEOD-28520 | biostudies-arrayexpress
Project description:We used microarrays to detail the global programme of gene expression underlying Polo-like kinase inhibition with BI 2536 compound in mouse bone marrow-derived dendritic cells (BMDCs) stimulated with Toll-like receptor agonists LPS and poly(I:C).
2011-04-12 | GSE28520 | GEO