E-MTAB-7279
Ontology highlight
ABSTRACT:
PROVIDER: E-MTAB-7279 | ExpressionAtlas | 2019-01-21
REPOSITORIES: ExpressionAtlas
Similar Datasets
Project description:Regional CNS immune fingerprint in chronic peripheral inflammation
| PRJEB29170 | ENA
Project description:Rheumatoid arthritis (RA) is linked to depression and dementia in later life by inflammatory involvement of the central nervous system (CNS). Regional heterogeneity of brain immunophenotypes was described under homeostasis, but a topographical resolution of CNS immune responses in chronic peripheral inflammatory diseases like RA is missing. We demonstrate regional heterogeneity of CNS susceptibility to chronic peripheral inflammation in the human tumor necrosis factor α transgenic (TNFtg) mouse model of RA. TNFtg mice showed myeloid cell infiltration, microglial activation, and a mutual transcriptomic fingerprint of neuroinflammation in the cortex, striatum, and thalamus. Immune responses were minimal in the hippocampus and cerebellum. We demonstrate regional CNS immune responses to chronic peripheral inflammation, sparing the hippocampus and cerebellum and reversible by peripheral anti-inflammatory treatment. Targeting microenvironmental susceptibility or resilience of brain regions will help to prevent and treat RA-related neuropsychiatric comorbidity. RNA-sequencing was performed from five brain regions (cortex, striatum, thalamus, hippocampus, and cerebellum) from C57Bl6/J wild type mice and TNFtg mice (strain Tg197; kindly provided by George Kollias (Fleming Institute, Vari, Greece).
2018-10-22 | E-MTAB-7279 | biostudies-arrayexpress
Project description:Systemic immune dysregulation contributes to the development of neuropsychiatric and neurodegenerative diseases. The precise effect of chronic peripheral immune stimulation on myeloid cells across anatomical brain regions is unclear. We used the human TNF-α transgenic mouse model of RA (TNFtg mice, strain Tg197) (Keffer et al., 1991), which shows increased levels of peripheral cytokines and severe joint pathology at young age and leads to severe disability within 3-4 months after birth (Keffer et al., 1991; Suss et al., 2015) to assess the effect of chronic peripheral inflammation on myeloid cells in the cortex. To examine the response of brain myeloid cells to systemic chronic inflammation, we performed single cell RNA-seq on isolated CD11b+CD45+ cells from the cortex of wt and TNFtg mice.
2020-03-14 | GSE145708 | GEO
Project description:<p>Rheumatoid arthritis (RA) is a chronic inflammatory disorder with poorly defined aetiology characterised by synovial inflammation with variable disease severity and drug responsiveness. To investigate the peripheral blood immune cell landscape of RA, we performed comprehensive clinical and molecular profiling of 267 RA patients and 52 healthy vaccine recipients for up to 18 months to establish a high quality sample biobank including plasma, serum, peripheral blood cells, urine, genomic DNA, RNA from whole blood, lymphocyte and monocyte subsets. We have performed extensive multi-omic immune phenotyping, including genomic, metabolomic, proteomic, transcriptomic and autoantibody profiling. We anticipate that these detailed clinical and molecular data will serve as a fundamental resource offering insights into immune-mediated disease pathogenesis, progression and therapeutic response, ultimately contributing to the development and application of targeted therapies for RA.</p>
2021-06-16 | MTBLS1497 | MetaboLights
Project description:Chronic pain is one of the most significant and costly medical problems throughout the world. Recent evidence has confirmed the hippocampus as an active modulator of pain chronicity but the underlying mechanisms remain poorly defined. By means of in vivo electrophysiology together with chemogenetic and optogenetic manipulations in freely behaving mice, we identified a neural ensemble in the ventral hippocampal CA1 (vCA1) that showed inhibitory responses to noxious external stimuli, but not to innocuous stimuli. Following peripheral inflammation, this neuronal ensemble became responsive to innocuous stimuli and causally contributed to sensory hypersensitivity in inflammatory animals. Mimicking this inhibition of vCA1 neurons using chemogenetics in naïve mice induced chronic pain-like behavioral changes, whereas activating these vCA1 neurons in mice with chronic peripheral inflammation resulted in a striking reduction of pain-related behaviors. Pathway-specific manipulation of vCA1 projections to the basolateral amygdala (BLA) and infralimbic cortex (IL) showed that these pathways were differentially involved in pain modulation at different temporal stages of chronic inflammatory pain. These results confirm a crucial role of the ventral hippocampus and its circuits in modulating the development of chronic pain in mice.
2022-12-19 | PXD038416 | Pride
Project description:Peripheral inflammation has been associated with various neurodegeneration, including Alzheimer's Disease (AD). In this study, we employed an AD mouse model nasally infected with Staphylococcus aureus to assess the impact of chronic or acute peripheral inflammation on brain transcriptome and amyloid pathology. The chronic exposure increased the diffuse and compact amyloid plaques and blood cytokine levels. Following a short-term exposure, single-cell and spatial transcriptomics uncovered cell type- and spatial-specific transcriptional changes indicating a dysregulation of the brain barriers, including the blood-brain and the blood-cerebrospinal fluid barriers. Brain macrophages exhibited increased Apoe expression and macrophage-specific genes were upregulated at ventricular areas of infected mice. In addition, we report an increase of disease associated microglia genes around the A plaques, together with disbalances in neuronal expression in response to peripheral inflammation. Overall, results enlighten the mechanisms linking peripheral inflammation to AD.
2023-07-15 | GSE218360 | GEO
Project description:Peripheral inflammation has been associated with various neurodegeneration, including Alzheimer's Disease (AD). In this study, we employed an AD mouse model nasally infected with Staphylococcus aureus to assess the impact of chronic or acute peripheral inflammation on brain transcriptome and amyloid pathology. The chronic exposure increased the diffuse and compact amyloid plaques and blood cytokine levels. Following a short-term exposure, single-cell and spatial transcriptomics uncovered cell type- and spatial-specific transcriptional changes indicating a dysregulation of the brain barriers, including the blood-brain and the blood-cerebrospinal fluid barriers. Brain macrophages exhibited increased Apoe expression and macrophage-specific genes were upregulated at ventricular areas of infected mice. In addition, we report an increase of disease associated microglia genes around the A plaques, together with disbalances in neuronal expression in response to peripheral inflammation. Overall, results enlighten the mechanisms linking peripheral inflammation to AD.
2023-07-15 | GSE218352 | GEO
Project description:Peripheral inflammation has been associated with various neurodegeneration, including Alzheimer's Disease (AD). In this study, we employed an AD mouse model nasally infected with Staphylococcus aureus to assess the impact of chronic or acute peripheral inflammation on brain transcriptome and amyloid pathology. The chronic exposure increased the diffuse and compact amyloid plaques and blood cytokine levels. Following a short-term exposure, single-cell and spatial transcriptomics uncovered cell type- and spatial-specific transcriptional changes indicating a dysregulation of the brain barriers, including the blood-brain and the blood-cerebrospinal fluid barriers. Brain macrophages exhibited increased Apoe expression and macrophage-specific genes were upregulated at ventricular areas of infected mice. In addition, we report an increase of disease associated microglia genes around the A plaques, together with disbalances in neuronal expression in response to peripheral inflammation. Overall, results enlighten the mechanisms linking peripheral inflammation to AD.
2023-07-15 | GSE218346 | GEO
Project description:Inflammation plays a role in neuropathic pain conditions as well as in pain induced solely by an inflammatory stimulus. Robust mechanical hyperalgesia and allodynia can be induced by locally inflaming the L5 dorsal root ganglion (DRG) in rat. This model allows investigation of the contribution of inflammation per se to chronic pain conditions. Most previous microarray studies of DRG gene expression have investigated neuropathic pain models involving axon transection. To examine the role of inflammation, we used microarray methods to examine gene expression 3 days after local inflammation of the L5 DRG in rat. We observed significant regulation in a large number of genes (23% of observed transcripts), and examined 221 (3%) with a fold-change of 1.5-fold or more in more detail. Immune-related genes were the largest category in this group and included members of the complement system as well as several pro-inflammatory cytokines. However, these upregulated cytokines had no prior links to peripheral pain in the literature other than through microarray studies, though most had previously described roles in CNS (especially neuroinflammatory conditions) as well as in immune responses. The L5 dorsal root ganglion (DRG) was locally inflamed with zymosan/Incomplete Freund's Adjuvant. DRG were isolated 3 days later. Each sample was RNA extracted from a single DRG. 6 samples from rats with local DRG inflammation were compared with 6 samples from sham-operated rats.
2012-06-21 | E-GEOD-38859 | biostudies-arrayexpress