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CCL7 promotes macrophage polarization and synovitis to exacerbate rheumatoid arthritis II

ABSTRACT: CCL7 promotes macrophage polarization and synovitis to exacerbate rheumatoid arthritis II

PROVIDER: PRJNA1207088 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31907041_1.fastq.gz	Fastqsanger.gz
	SRR31907041_2.fastq.gz	Fastqsanger.gz
	SRR31907042_1.fastq.gz	Fastqsanger.gz
	SRR31907042_2.fastq.gz	Fastqsanger.gz
	SRR31907043_1.fastq.gz	Fastqsanger.gz

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CCL7 promotes macrophage polarization and synovitis to exacerbate rheumatoid arthritis

Project description:Macrophage polarization and synovitis play significant roles in rheumatoid arthritis (RA). Chemokines are involved almost throughout the entire pathology of synovitis. However, the interaction between chemokines and macrophage polarization in RA has been seldom reported. This study found that chemokine C-C motif ligand 7 (CCL7) secreted by polarized M1 macrophages enhances M1 polarization, creating a positive feedback loop and revealing the role of CCL7 in the progression of rheumatoid arthritis. In this research, RNA sequencing indicated that M1 polarized macrophages secrete a large amount of CCL7, which further enhances M1 polarization. Through immunohistochemistry and enzyme-linked immunosorbent assay, it was found that the expression of CCL7 in the synovial tissue and serum of RA patients and mice was upregulated. Intra-articular injection of CCL7 recombinant protein exacerbated M1 polarization of macrophages, inflammation, fibrosis in the synovial tissue, and worsened arthritis pain in mice, which was improved after the injection of CCL7 neutralizing antibody. In addition, CCL7 promoted M1 polarization of macrophages and reversed the M2 polarization induced by IL-4, and it also promoted macrophage proliferation and migration. Although it had an inhibitory effect on chondrocyte activity, it did not show a significant impact on chondrocyte metabolism. Mechanistically, CCL7 targets CCR1 to promote M1 polarization of macrophages, a process partly mediated through the activation of the JAK2/STAT1 pathway. When stimulated by CCL7, macrophages secreted a vast amount of pro-inflammatory factors, exacerbating synovitis and cartilage damage, leading to the aggravation of RA disease. Our research established a positive feedback loop between M1 polarization of macrophages and CCL7, indicating that blocking CCL7 could improve the progression of RA, suggesting CCL7 as a potential target for RA treatment.

2025-01-08 | GSE267151 | GEO

CCL7 promotes macrophage polarization and synovitis to exacerbate rheumatoid arthritis II

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CCL7 promotes macrophage polarization and synovitis to exacerbate rheumatoid arthritis

Project description:CCL7 promotes macrophage polarization and synovitis to exacerbate rheumatoid arthritis

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CCL7 promotes macrophage polarization and synovitis to exacerbate rheumatoid arthritis.

Project description: Not available

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Disease activity drives transcriptomic heterogeneity in early untreated rheumatoid synovitis

Project description:Disease activity drives transcriptomic heterogeneity in early untreated rheumatoid synovitis

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ATAC-seq of synovial tissues from mice with Antigen Induced Arthritis (AIA) showing distinct hallmarks of synovitis heterogeneity

Project description:Joint pathology in rheumatoid arthritis is broadly classified as fibroblast-rich, myeloid-rich, or lymphoid-rich synovitis. How these pathotypes evolve is unknown. Based on the clinical efficacy of biological medicines and targeted inhibitors, we hypothesise that cytokines instruct this process, affecting the rate of onset, severity, and course of disease. These include cytokine signals that define the organisation and maintenance of lymphocyte sentinels in lymphoid-rich synovitis, and others that guide a pauci-immune pathology involving activated stromal cells in fibroblast-rich synovitis. With a long-standing interest in the IL-6 cytokine family, we have identified distinct roles for Jak-STAT signalling in shaping synovitis heterogeneity. Establishing new mouse models that mimic fibroblast-rich, myeloid-rich, and lymphoid-rich synovitis in humans, we propose that wild-type (WT), Il6ra-/-, and Il27ra-/- mice with AIA share hallmarks of these pathotypes. The reported RNA-seq now profiles the transcriptional profile of synovitis in WT, Il6ra-/-, and Il27ra-/- mice with AIA and provides datasets captured at day-3 and day-10 AIA reflecting early and established disease.

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Bulk RNA-seq of synovial tissues from mice with Antigen Induced Arthritis (AIA) showing distinct hallmarks of synovitis heterogeneity

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Disease activity drives transcriptomic heterogeneity in early untreated rheumatoid synovitis

Project description:The purpose of this study was to investigate the transcriptomic heterogeneity in synovial tissue of early untreated rheumatoid arthritis patients in association with clinical data

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Project description:Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by synovitis and/or joint deterioration. Interstitial lung disease (ILD) is one of extra-articular manifestations of RA characterized by inflammation and/or fibrosis. Clinically relevant rheumatoid arthritis-related interstitial lung disease (RA-ILD) occurs in 10% of RA patients and is associated with poor prognosis. Although a poor prognosis has been reported, little is known about RA-ILD. Here, we report the first detailed transcriptomic analysis of the epithelial and immune cell populations in RA-ILD lungs at the single-cell level.

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Project description: Not available

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