Transcriptomic characterization of classical monocytes highlights the involvement of immuno-inflammation in bone erosion in Rheumatoid Arthritis
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ABSTRACT:
PROVIDER: PRJEB66223 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR12063400.fastq.gz | Fastqsanger.gz | |||
| ERR12063342.fastq.gz | Fastqsanger.gz | |||
| ERR12063343.fastq.gz | Fastqsanger.gz | |||
| ERR12063344.fastq.gz | Fastqsanger.gz | |||
| ERR12063345.fastq.gz | Fastqsanger.gz |
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Project description:Rheumatoid arthritis (RA) is a chronic inflammatory disease associated with localized bone involvement characterized by the presence of bone erosions. Evidence-based data suggest that under inflammatory conditions, classical monocytes are the main source of osteoclasts and might be involved in bone erosion pathophysiology. Here, we analyze the transcriptomic profile of classical monocytes in erosive and non-erosive rheumatoid arthritis patients in order to better understand their contribution to bone erosion. Thirty-nine premenopausal RA patients and 20 healthy age-matched women were recruited for this study. Classical monocytes were isolated from peripheral blood through negative selection. Sequencing library was constructed using the Quant-seq® 30 mRNA-Seq Library Prep Kit (Lexogen®) and sequenced using an Illumina Seq 2500 platform (Illumina®). Differential expression analysis was performed between patients and control groups. Therefore, gene sets analysis was performed to identify the enriched biological pathways. Results suggested that alterations in pathways related to the inflammatory process and impairment of bone formation have an important role in the pathophysiology of bone erosions in patients with rheumatoid arthritis.
2023-09-19 | E-MTAB-13361 | biostudies-arrayexpress
Project description:IntroductionEvidence-based data suggest that under inflammatory conditions, classical monocytes are the main source of osteoclasts and might be involved in bone erosion pathophysiology. Here, we analyze the transcriptomic profile of classical monocytes in erosive and non-erosive rheumatoid arthritis patients in order to better understand their contribution to bone erosion.MethodsThirty-nine premenopausal RA patients were consecutively enrolled and divided into two groups based on the presence of bone erosions on hand joints. Classical monocytes were isolated from peripheral blood through negative selection, and RNA-seq was performed using a poly-A enrichment kit and Illumina® platform. Classical monocytes transcriptome from healthy age-matched women were also included to identify differentially expressed genes (DEGs). Therefore, gene sets analysis was performed to identify the enriched biological pathways.ResultsRNA-seq analysis resulted in the identification of 1,140 DEGs of which 89 were up-regulated and 1,051 down-regulated in RA patients with bone erosion compared to those without bone erosions. Among up-regulated genes, there was a highlighted expression of IL18RAP and KLF14 related to the production of pro-inflammatory cytokines, innate and adaptive immune response. Genes related to collagen metabolism (LARP6) and bone formation process (PAPPA) were down-regulated in RA patients with erosions. Enriched pathways in patients with erosions were associated with greater activation of immune activation, and inflammation. Interestingly, pathways associated with osteoblast differentiation and regulation of Wnt signaling were less activated in RA patients with erosions.ConclusionThese findings suggest that alterations in expression of monocyte genes related to the inflammatory process and impairment of bone formation might have an important role in the pathophysiology of bone erosions in RA patients.
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Project description:Rheumatoid arthritis (RA) patients may display atypical CD21-/lo B cells in their blood but the significance of this observation remains unclear. We report here that the group of RA patients with elevated frequencies of CD21-/lo B cells shows decreased ataxia-telangiectasia mutated (ATM) expression and activation in B cells compared with other RA patients and healthy donor controls. In agreement with ATM involvement in the regulation of V(D)J recombination, RA patients with defective ATM function displayed a skewed B cell receptor (BCR) Igk repertoire, which resembled that of ataxia-telangiectasia (AT) patients. This repertoire was characterized by increased Jk1 and decreased upstream Vk gene segment usage, suggesting improper secondary recombination processes and selection. In addition, altered ATM function in B cells was associated with decreased osteoprotegerin (OPG) and increased RANKL production. These changes favor bone loss and correlated with a higher prevalence of erosive disease in RA patients with impaired ATM function. Using a humanized mouse model, we also show that ATM inhibition in vivo induces an altered Igk repertoire and RANKL production by immature B cells in the bone marrow, leading to decreased bone density. We conclude that dysregulated ATM function in B cells promotes bone erosion and the emergence of circulating CD21-/lo B cells, thereby contributing to RA pathophysiology.
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Project description:Polyarticular Juvenile Idiopathic Arthritis (pJIA) is a childhood-onset autoimmune disease. Immune cells contribute to persistent inflammation observed in pJIA. Despite the crucial roleof monocytes in arthritis, the precise involvement of classical monocytes in the pathogenesis of pJIA remains uncertain. Here, we aimed to uncover the transcriptomic patterns of classical monocytes in pJIA, focusing on their involvement in disease mechanism and heterogeneity. Seventeen healthy subjects and eighteen premenopausal women with pJIA according to ILAR criteria were included. Classical monocytes were isolated and RNA sequencing was performed. Differential expression analysis was used to compare pJIA patients and healthy control group. Differentially expressed genes (DEGs) were identified and gene set enrichment analysis (GSEA) was performed. Using unsupervised learning approach, patients were clustered in two groups based on their similarities at transcriptomic level. Subsequently, these clusters underwent a comparative analysis to reveal differences at the transcriptomic level. We identified 440 DEGs in pJIA patients of which 360 were up-regulated and 80 down-regulated. GSEA highlighted TNF- and IFN- response. Importantly, this analysis detected genes targeted by pJIA therapy, but also identified new modulators of immuno-inflammation. PLAUR, IL1B, IL6, CDKN1A, PIM1 and ICAM1 were pointed as drivers of chronic hyperinflammation. Unsupervised learning approach revealed two clusters within pJIA, each exhibiting varying inflammation levels. These findings indicate the pivotal role of immuno-inflammation driven by classical monocytes in pJIA and reveals the existence of two subclusters within pJIA, regardless the positivity of rheumatoid factor and anti-CCP, paving the way to precision medicine.
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