Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA283833 | ENA |
REPOSITORIES: ENA
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Project description:To evaluate DR?1-mMOG-35-55 effects on CNS inflammation during Experimental allergic encephalomyelitis (EAE) in a more comprehensive manner, we performed microarray analysis on spinal cords from DR?1-mMOG-35-55- vs. Vehicle-treated DR*1501-Tg mice with EAE. EAE was induced with mMOG-35-55/CFA/Ptx and mice were treated with DR?1-mMOG-35-55 (100ug daily x 3) or Vehicle ,after disease onset at a clinical score of 2. Twenty four hr after the last treatment, total RNA was isolated from spinal cords and gene expression profiles from pooled RNA were analyzed using the Mouse Gene 2.0 ST Affymetrix GeneChip system RNA was isolated from spinal cords of 3 DRa1-mMOG-35-55 treated mice and 3 Vehicle treated mice,and pooled in to two groups SCV - for Vheicle treatment and SCA - for DRa1-mMOG-35-55 treatment
2015-05-13 | E-GEOD-68805 | biostudies-arrayexpress
Project description:To evaluate DRα1-mMOG-35-55 effects on CNS inflammation during Experimental allergic encephalomyelitis (EAE) in a more comprehensive manner, we performed microarray analysis on spinal cords from DRα1-mMOG-35-55- vs. Vehicle-treated DR*1501-Tg mice with EAE. EAE was induced with mMOG-35-55/CFA/Ptx and mice were treated with DRα1-mMOG-35-55 (100ug daily x 3) or Vehicle ,after disease onset at a clinical score of 2. Twenty four hr after the last treatment, total RNA was isolated from spinal cords and gene expression profiles from pooled RNA were analyzed using the Mouse Gene 2.0 ST Affymetrix GeneChip system
2015-05-13 | GSE68805 | GEO
Project description:The study assessed the efficacy of R-flurbiprofen in experimental autoimmune encephalomyelitis (EAE) models of multiple sclerosis in mice. R-flurbiprofen, also known as tarenflurbil, is the R-enantiomer of the cyclooxyygenase inhibitor S-flurbiprofen. It is ineffective in terms of cyclooxygenase inhibition and has no relevant toxicity in humans. Oral R-flurbiprofen prevented and attenuated primary progressive EAE in C57BL6/J mice and relapsing-remitting EAE in SJL mice, even if the treatment was initiated on or after the first flare of the disease. R-flurbiprofen reduced immune cell infiltration and microglia activation and inflammation in the spinal cord, brain and optic nerve and attenuated myelin destruction and EAE-evoked hyperalgesia. R-flurbiprofen treatment increased CD4+CD25+FoxP3+ regulatory T-cells, CTLA4+ inhibitory T-cells and interleukin-10, whereas the EAE-evoked upregulation of pro-inflammatory genes in the spinal cord was strongly reduced (Sentrix6 results). The effects were associated with an increase of plasma and cortical endocannabinoids but decreased spinal prostaglandins, the latter likely due to R- to S inversion. The promising results suggest potential efficacy of R-flurbiprofen in human MS. To assess effects of R-flurbiprofen on EAE evoked gene regulations in the spinal cord a genome wide expression analysis was performed using Illumina Sentrix 6 v2 BeadChips. For the microarray study female C57BL6/J mice were immunized according to a standard protocol using the Hooke KitM-bM-^DM-" MOG35-55/CFA emulsion PTX (EK-2110, Hooke Labs, St Lawrence, MA), which contains 200 M-BM-5g myelin oligodendrocyte glycoprotein (MOG) 35-55 emulsified in 200 M-BM-5l Complete FreundM-bM-^@M-^Ys Adjuvant (CFA). The emulsion was injected subcutaneously at two sites followed by two intraperitoneal (i.p.) injections of 200 ng pertussis toxin (PTX) in phosphate buffered saline (PBS), the first 1-2 h after MOG35-55, and the second 24 h after MOG35-55. Control mice received CFA without MOG35-55 (sham mice). Treatment with R-flurbiprofen or vehicle (n = 12 per group) was started 5 days after immunization and was administered continuously via the drinking water up to the end. Spinal cords were dissected out during the flare of the disease, day 16 after immunization. For microarray analysis, total RNA was extracted from homogenizedlumbar spinal cord tissue with Trizol reagent, followed by clean-up and DNase I treatment with QIAGEN RNeasy mini kit. RNA quality was checked (Nanodrop ND-1000, Agilent 2100 Bioanalyzer), and subsequently biotinylated and hybridized to Mouse Sentrix-6 V2 Expression BeadChips (Illumina). Each sample consisted of pooled lumbar spinal cord tissue from 3 animals and 3 replicate samples were analyzed per group, i.e. the analysis is based on 9 mice per group. Groups were CFA-control with vehicle treatment, CFA-control with R-flurbiprofen, EAE-vehicle and EAE-R-flurbiprofen treatment. Treatment was started 5 days after immunization. For dissection, pairs were matched according to the clinical scores. QC, labeling, hybridization and raw data evaluation and normalization were done according to standard protocols at the core facilities of the Deutsche Krebsforschungszentrum, Heidelberg, Germany.
2014-08-28 | E-GEOD-60847 | biostudies-arrayexpress
Project description:Gene expression analysis in the spinal cord and brain of vehicle-treated and ORY-2001 and ORY-LSD1 treated EAE mice in the subchronic (SC) and of ORY-2001 and ORY-LSD1 in the effector (E) phase in EAE mice
2021-08-03 | GSE118071 | GEO
Project description:The study assessed the efficacy of R-flurbiprofen in experimental autoimmune encephalomyelitis (EAE) models of multiple sclerosis in mice. R-flurbiprofen, also known as tarenflurbil, is the R-enantiomer of the cyclooxyygenase inhibitor S-flurbiprofen. It is ineffective in terms of cyclooxygenase inhibition and has no relevant toxicity in humans. Oral R-flurbiprofen prevented and attenuated primary progressive EAE in C57BL6/J mice and relapsing-remitting EAE in SJL mice, even if the treatment was initiated on or after the first flare of the disease. R-flurbiprofen reduced immune cell infiltration and microglia activation and inflammation in the spinal cord, brain and optic nerve and attenuated myelin destruction and EAE-evoked hyperalgesia. R-flurbiprofen treatment increased CD4+CD25+FoxP3+ regulatory T-cells, CTLA4+ inhibitory T-cells and interleukin-10, whereas the EAE-evoked upregulation of pro-inflammatory genes in the spinal cord was strongly reduced (Sentrix6 results). The effects were associated with an increase of plasma and cortical endocannabinoids but decreased spinal prostaglandins, the latter likely due to R- to S inversion. The promising results suggest potential efficacy of R-flurbiprofen in human MS. To assess effects of R-flurbiprofen on EAE evoked gene regulations in the spinal cord a genome wide expression analysis was performed using Illumina Sentrix 6 v2 BeadChips. For the microarray study female C57BL6/J mice were immunized according to a standard protocol using the Hooke Kit™ MOG35-55/CFA emulsion PTX (EK-2110, Hooke Labs, St Lawrence, MA), which contains 200 µg myelin oligodendrocyte glycoprotein (MOG) 35-55 emulsified in 200 µl Complete Freund’s Adjuvant (CFA). The emulsion was injected subcutaneously at two sites followed by two intraperitoneal (i.p.) injections of 200 ng pertussis toxin (PTX) in phosphate buffered saline (PBS), the first 1-2 h after MOG35-55, and the second 24 h after MOG35-55. Control mice received CFA without MOG35-55 (sham mice). Treatment with R-flurbiprofen or vehicle (n = 12 per group) was started 5 days after immunization and was administered continuously via the drinking water up to the end. Spinal cords were dissected out during the flare of the disease, day 16 after immunization.
2014-08-28 | GSE60847 | GEO
Project description:We have discovered that neutrophils that infiltrate the spinal cord of mice with EAE, a model of multiple sclerosis, but not intravascular neutrophils that crawl on the luminal endothelial surface, bear on their surface the adhesion molecule Icam1. The goal of this experiment was to use Icam1 to isolate these two neutrophil subpopulations in order to compare their transcriptomes and gain insights into their properties. To this end, EAE was induced in C57BL/6J mice by immunization with myelin oligodendrocyte glycoprotein (MOG) peptide (a.a. 35-55) and adjuvants (i.e. complete Freund’s adjuvant and pertussis toxin). On day 15 post-immunization, intravascular neutrophils (CD45hiCD11b+CD11c−Ly6g+Icam1−) and extravasated neutrophils (CD45hiCD11b+CD11c−Ly6g+Icam1+) were isolated from spinal cords by FACS. For comparison, we simultaneously isolated two other populations of myeloid cells: macrophages (CD45hiCD11b+CD11c−Ly6g−) and dendritic cells (CD45hiCD11b+CD11c+Ly6g−). RNA was analyzed in biological duplicate using Affymetrix GeneChip Mouse Gene 2.0 ST arrays.
2017-11-10 | E-MTAB-6160 | biostudies-arrayexpress
Project description:We performed micrarrays to investigate neuronal gene expression changes during acute inflammatory CNS axon injury using the murine myelin oligodendrocyte glycoprotein 35-55 (MOG35-55)-induced experimental autoimmune encephalomyelitis (EAE) model. The present study was assigned to assess the direct and indirect endogenous neuronal response to spinal axonal injury in the motor and sensory cortex.
2014-10-01 | GSE47900 | GEO
Project description:We performed micrarrays to investigate neuronal gene expression changes during acute inflammatory CNS axon injury using the murine myelin oligodendrocyte glycoprotein 35-55 (MOG35-55)-induced experimental autoimmune encephalomyelitis (EAE) model. The present study was assigned to assess the direct and indirect endogenous neuronal response to spinal axonal injury in the motor and sensory cortex. Gene expression in motor and sensory cortex enriched tissue was assessed from four healthy and six EAE female mice. Tissue was collected from mice with paraplegia or monoplegia, with contralateral hindlimb paresis (EAE day 18-21). The gene expression profiles of the EAE mice were compared to the motor or sensory cortex of healthy control mice, resulting in a list of differentially expressed genes in healthy and EAE mice.
2014-10-01 | E-GEOD-47900 | biostudies-arrayexpress
Project description:Multiple sclerosis (MS) is an autoimmune disease of the central nervous system (CNS); its cause is unknown. To understand the pathogenesis of MS, researchers often use the experimental autoimmune encephalomyelitis (EAE) mouse model. Here, our aim was to build a proteome map of the biological changes that occur during MS at the major onset sites—the brain and the spinal cord. We performed quantitative proteome profiling in five specific brain regions and the spinal cord of EAE and healthy mice with high-resolution mass spectrometry based on tandem mass tags.
2019-02-25 | PXD011428 | Pride
Project description:Tregs and Tcons were isolated by flow cytometry from the spleen of naïve mice and from the spleen and central nervous system (brain + spinal cord) (CNS) of mice at the peak of experimental autoimmune encephalomyelitis (EAE) induced by immunization with MOG(35-55). Samples at EAE peak were collected at day 16-18 after immunization. Purity was >99.5%. Foxp3.eGFP mice (provided by A. Rudensky) were used to identify Tregs. A bin channel excluded CD11b+ cells during the sort. Mice were 6-10 weeks of age at the time of immunization. The goal was to identify genes differentially expressed between Tregs and Tcons from naive mice, and genes differentially expressed by these cells in the inflamed tissue (central nervous system) at the peak of the disease.
2022-10-12 | GSE164460 | GEO