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Effect of anti-mouse TNF and IL-6 antibodies as well as their combination in a collagen-induced arthritis mouse model

ABSTRACT: Additive effects of anti-TNF and anti-IL-6 were evaluated in a murine collagen-induced arthritis (CIA) model by RNA-seq

ORGANISM(S): Mus musculus

PROVIDER: GSE200292 | GEO | 2022/12/31

REPOSITORIES: GEO

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Collagen induced arthritis plasma proteomic analysis

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).

2020-09-18 | PXD015274 | Pride

Effect of anti-mouse TNF and IL-6 antibodies as well as their combination in a collagen-induced arthritis mouse model

Project description:Effect of anti-mouse TNF and IL-6 antibodies as well as their combination in a collagen-induced arthritis mouse model

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Transcription profiling of mouse knee joint synovium from different grades of inflammation in mouse collagen induced arthritis (CIA)

Project description:Knee joint synovium was used for gene expression analysis of mouse collagen induced arthritis (CIA). Synovium was prepared at day 30 after initial sensitization from: healthy controls, CIA animals with no, with mild, with moderate, or with severe joint inflammation. Each sample group is represented by three replicates, each consisting of tissue collected from three to four animals. Experiment Overall Design: The data set consists of 15 samples: five groups with three replicates each. One sample group is from healthy controls, the other groups are from CIA animals with different degress of joint inflammation.

2009-09-15 | E-GEOD-13071 | biostudies-arrayexpress

Knee joint synovium from different grades of inflammation in mouse collagen induced arthritis (CIA)

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Multi-organ single cell analysis of a mouse model of collagen-induced arthritis [subseries1]

Project description:Prioratization of disease associated mechanisms in immune-mediated inflammatory diseases (IMIDs) is complicated by altered interactions across multiple organs and cell types. We have adressed these challenges by analyzing a multi-organ multicellular disease model (MO-MCDM) of a mouse IMID model, namely collagen-induced arthritis (CIA). For all the five organs (joint, lung, muscle, skin, and spleen) we found highly complex and heterogenous expression changes due to disease, although, macroscopic and microscopic signs of inflammation could only be seen in joints. Based on the MO-MCDM, predicted molecular interactions within and between organs could be identified. The model supported that inflammation was switched on or off in different organs, by an altered balande between pro- and anti-inflammatory upstream regulators and downstream pathways. This on/off switch was validated in human IMIDs, by analyses of publically available data from 32 different samples of 10 different IMIDs. Additionally, it showed consistency with a general characteristic of both CIA and human IMIDs, namely variable organ involvement in disease.

2023-01-31 | GSE206651 | GEO

Bulk RNA-seq on paws of collagen-induced arthritis (CIA) mouse model at different disease stages

Project description:The goal of this experiment is to profile longitudinal transcriptome changes during the development of murine arthritis in CIA mouse model. Male DBA1 mice (age between 10 to 12 weeks) were used in this study. CIA was induced by two immunizations with Type II collagen in Complete Freund’s adjuvant (CFA) at day 0, and with Type II collagen in Incomplete Freund’s adjuvant (IFA) at day 21. Bulk RNA-seq were done on right hind paws from control (non-immunized DBA1 mice) and CIA mice at different disease stages (up to 10 weeks after 1st immunization).

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Time-course gene expression profiles of the synovial tissues in collagen-induced arthritis

Project description:We observed resolution of inflammatory response in collagen-induced arthritis (CIA) mice. To identify molecular signatures defining resolution of the CIA, we applied microarray analysis for synovial tissues in the CIA mice in 6 (induction), 9 (peak) and 15 weeks (resolution) after immunization. To identify genes related to CIA resolution, we performed the following comparisons of gene expression profiles: peak versus induction phase and resolution versus peak phase. We identified that three genes, Itgb1, Ywhaz and Rps3, are the key regulators for the resolution by measuring degree, betweenness and closeness centrality in reconstructed network based on protein-protein interaction data. To confirm this result, we compared the gene and protein expression level of the three regulators between the two phases of inflammation. Furthermore, we showed that the gene and protein expression level of the three regulators are up-regulated in regulatory T cells and type 2 macrophages than other subtypes of CD4+ T cells and macrophages, and also we examined that recombinant peritoneal macrophages of the three regulators can modulate the expression of pro-inflammatory and anti-inflammatory cytokines. Thus, our findings suggest that those regulators can be employed as therapeutic uses for resolving inflammation

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miRNAs expression in joint of Collagen-induced arthritis (CIA)

Project description:MicroRNAs (miRNAs) have been implicated as fine-tuning regulators controlling diverse biological processes at the level of posttranscriptional repression. Dysregulation of miRNAs has been described in various disease states, including inflammatory autoimmune diseases. By using high-throughput microRNA profiling analysis, we identified a series of miRNAs dysregulated in local inflammatory lesions of human patients with autoimmune diseases, as well as their relevant mouse models such as CIA. We isolated joint samples pooled from six CIA mice or from six naM-CM-/ve control mice. Total RNA was extracted for the TaqManM-BM-. Low Density Assay v3.0

2012-12-19 | E-GEOD-37422 | biostudies-arrayexpress

Multi-organ single cell analysis of a mouse model of collagen-induced arthritis [subseries2]

Project description:Prioratization of disease associated mechanisms in immune-mediated inflammatory diseases (IMIDs) is complicated by altered interactions across multiple organs and cell types. We have adressed these challenges by analyzing a multi-organ multicellular disease model (MO-MCDM) of a mouse IMID model, namely collagen-induced arthritis (CIA). In this pilot study, we sequenced at least one healthy and one CIA sample from each of the ten organs, joint, lung, muscle, skin, spleen, blood, draining lymph nodes, thymus, liver, and kidney. Sequencing data from liver and kidney never reached our defined quality cut-off, and were thus excluded from further comparisions. Of the remaining organs, we found that joint, lung, muscle, skin, and spleen had the highest number of DEGs between CIA and healthy mice. We thus reason that these five organs shoult be most relevant to study disease associated changes on a systemic level, and prioritized those for further analyses.

2023-01-31 | GSE206654 | GEO

Microbiota-dependent indole production is required for the development of collagen-induced arthritis

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.

2023-11-13 | GSE241655 | GEO

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