Exploring the transcriptome of resident spinal microglia after collagen antibody-induced arthritis
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ABSTRACT:
PROVIDER: PRJNA429039 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR6450880_1.fastq.gz | Fastqsanger.gz | |||
| SRR6450880_2.fastq.gz | Fastqsanger.gz | |||
| SRR6450890_1.fastq.gz | Fastqsanger.gz | |||
| SRR6450890_2.fastq.gz | Fastqsanger.gz | |||
| SRR6450900_1.fastq.gz | Fastqsanger.gz |
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Project description:Microglia have emerged as crucial players in the maintenance of mechanical hypersensitivity in models of chronic pain, including rheumatoid arthritis. Recent studies have suggested that there is a sexually dimorphic microglial involvement in chronic pain, but the debate is still ongoing. Here, we have used the collagen antibody-induced arthritis (CAIA) mouse model to ascertain possible differences between male and female microglia in the context of arthritis-induced pain. We have focused on the late phase of this arthritis model, when joint inflammation has resolved but mechanical hypersensitivity and microglial activation persist. We found that intrathecal administration of minocycline reversed mechanical thresholds to control levels in male, but not female mice. Moreover, we isolated resident microglia from the lumbar dorsal horns of male and female mice and observed a significantly lower number of microglial cells in females by flow cytometry analysis. Furthermore, genome-wide RNA sequencing results pointed to several transcriptional differences between male and female microglia, but no convincing differences were identified between control and CAIA groups. Taken together, these findings suggest that there are significant but subtle sex differences in microglial expression profiles independent of treatment. To what extent they help bring about the behavioural sexual dimorphism observed after minocycline administration remains to be explored. Finally, our experiments failed to identify the underlying biological correlates of the microglial activation that is present in the late phase of the CAIA model. It is likely that transcriptional changes are either subtle and highly localised and therefore difficult to identify with bulk isolation techniques or that other factors, such as changes in protein expression or epigenetic modifications are at play.
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Project description:Recent studies have suggested a sexually dimorphic role of spinal glial cells in the maintenance of mechanical hypersensitivity in rodent models of chronic pain. We have used the collagen antibody-induced arthritis (CAIA) mouse model to examine differences between males and females in the context of spinal regulation of arthritis-induced pain. We have focused on the late phase of this model when joint inflammation has resolved, but mechanical hypersensitivity persists. Although the intensity of substance P, calcitonin gene-related peptide, and galanin immunoreactivity in the spinal cord was not different from controls, the intensity of microglia (Iba-1) and astrocyte (glial fibrillary acidic protein) markers was elevated in both males and females. Intrathecal administration of the glial inhibitors minocycline and pentoxifylline reversed mechanical thresholds in male, but not in female mice. We isolated resident microglia from the lumbar dorsal horns and observed a significantly lower number of microglial cells in females by flow cytometry analysis. However, although genome-wide RNA sequencing results pointed to several transcriptional differences between male and female microglia, no convincing differences were identified between control and CAIA groups. Taken together, these findings suggest that there are subtle sex differences in microglial expression profiles independent of arthritis. Our experiments failed to identify the underlying mRNA correlates of microglial actions in the late phase of the CAIA model. It is likely that transcriptional changes are either subtle and highly localised and therefore difficult to identify with bulk isolation techniques or that other factors, such as changes in protein expression or epigenetic modifications, are at play.
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Project description:Time course of collagen-induced arthritis in DBA/1J male mice, synchronized on day 28 with 10ug LPS
2009-11-16 | E-TABM-661 | biostudies-arrayexpress
Project description:The aim of the project is to analyze the plasma proteomic profile of an animal model of arthritis (Collagen Induced Arthritis; CIA) in response to different treatments. For this, plasma samples from mice under five different treatments were analyzed (N=6 per group): Vehicle, CIA, CIA + Δ9-THCA-A (20 mg / kg), CIA + Δ9-THCA-A (20 mg / kg) + T0070907 (5 mg / kg) and CIA + Δ9-THCA-A (20 mg / kg) + SR141716A (5 mg / kg).
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Project description:The destruction of bone and cartilage results in a loss of joint functionality, critically impairing the quality of life in arthritis patients. Synovial fibroblasts (SFs) critically contribute to the pathogenesis of rheumatoid arthritis (RA) by acquiring either a pro-inflammatory or tissue-destructive phenotype. To explore the molecular mechanisms underlying the pathogenic fibroblast phenotype in arthritis, we performed single-cell RNA sequencing (scRNA-seq) on the synovial cells which were isolated from collagen-induced arthritis (CIA) mice.
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Project description:Oxylipins play important roles in various biological processes and are considered as mediators of inflammation for a wide range of diseases such as rheumatoid arthritis (RA). The purpose of this research was to study differences in oxylipin levels between a widely used collagen-induced arthritis (CIA) mice model and healthy control (Ctrl) mice. DBA/1J male mice (age: 6-7 weeks) were selected and randomly divided into two groups, viz. a CIA- and a Ctrl group. The CIA mice were injected intraperitoneal (i.p.) with the joint cartilage component collagen type II (CII) and an adjuvant injection of lipopolysaccharide (LPS). Oxylipin metabolites were extracted from plasma for each individual sample using solid phase extraction (SPE) and were detected with high performance liquid chromatography/tandem mass spectrometry (HPLC-ESI-MS/MS), using dynamic multiple reaction monitoring (dMRM). Both univariate and multivariate statistical analysis was applied. The results in univariate student's t-test revealed 10 significantly up- or down-regulated oxylipins in CIA mice, which were supplemented by another 6 additional oxylipins, contributing to group clustering upon multivariate analysis. The dysregulation of these oxylipins revealed the presence of ROS-generated oxylipins and an increase of inflammation in CIA mice. The results also suggested that the Collagen-induced arthritis might associate with dysregulation of apoptosis, possibly inhibited by activated NF- κ B because of insufficient PPAR-γ ligands.
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Project description:Altered tryptophan catabolism has been identified in inflammatory diseases like rheumatoid arthritis (RA) and spondyloarthritis (SpA), but the causal mechanisms linking tryptophan metabolites to disease are unknown. Using the collagen-induced arthritis (CIA) model we identify alterations in tryptophan metabolism, and specifically indole, that correlate with disease. We demonstrate that both bacteria and dietary tryptophan are required for disease, and indole supplementation is sufficient to induce disease in their absence. When mice with CIA on a low-tryptophan diet were supplemented with indole, we observed significant increases in serum IL-6, TNF, and IL-1β; splenic RORγt+CD4+ T cells and ex vivo collagen-stimulated IL-17 production; and a pattern of anti-collagen antibody isotype switching and glycosylation that corresponded with increased complement fixation. IL-23 neutralization reduced disease severity in indole-induced CIA. Finally, exposure of human colon lymphocytes to indole increased expression of genes involved in IL-17 signaling and plasma cell activation. Altogether, we propose a mechanism by which intestinal dysbiosis during inflammatory arthritis results in altered tryptophan catabolism, leading to indole stimulation of arthritis development. Blockade of indole generation may present a novel therapeutic pathway for RA and SpA.
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Project description:HIF2α works as an important transcription factor to induce target genes mediating cell proliferation, meabolism and inflammation. To gain new insights into HIF2α modulated genes, we used high-throughput sequencing to analyze potential HIF2a regulated genes in small intestine cells from collagen induced arthritis model mice.
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Project description:To determine te lncRNA expression profile in collagen-induced arthritis rats and normal rats, we uesed lncRNA microArray analysis form Arraystar to examine the expression of lncRNAs in CIA and normal rats' synovial tissues.
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Project description:Additive effects of anti-TNF and anti-IL-6 were evaluated in a murine collagen-induced arthritis (CIA) model by RNA-seq
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