Neutrophil extracellular traps (NETs) are increased in rheumatoid arthritis-associated interstitial lung disease DOI Creative Commons
Jing Xue,

Miaomiao Nian,

Yangyang Liang

et al.

Respiratory Research, Journal Year: 2025, Volume and Issue: 26(1)

Published: Jan. 22, 2025

Abstract Background Neutrophil extracellular trap (NET) formation has been implicated as a pathogenic mechanism in both rheumatoid arthritis (RA) and interstitial lung disease (ILD). However, the role of NETs RA-associated ILD (RA-ILD) mechanisms driving NET remain unclear. This study aimed to assess involvement RA-ILD elucidate underlying mechanisms. Methods Single-cell sequencing was used identify changes quantity function neutrophils tissue zymosan A (ZYM)-induced pneumonia model. Additionally, nuclear receptor 4A3 (NR4A3) interference performed HL-60 cells its impact on transformation MRC-5 into myofibroblasts. The clinical relevance plasma myeloperoxidase-DNA (MPO-DNA), citrullinated histone 3 (Cit-H3), cell-free DNA evaluated patients with different imaging types via commercial enzyme-linked immunosorbent assay (ELISA). Results In ZYM-treated SKG mouse model, which recapitulates key features RA-ILD, an increased population primarily responsible for formation. Mechanistically, we found that NR4A3 expression enhanced cells, turn promoted differentiation Clinically, MPO-DNA levels are elevated RA-nonspecific (RA-NSIP), whereas Cit-H3 RA-usual (RA-UIP) compared healthy subjects. ROC curve analysis further revealed combination MPO-DNA, factor (RF), anti-citrullinated protein (anti-CCP) Cit-H3, RF, anti-CCP were superior diagnostic panels NSIP UIP patients, respectively. Moreover, those from controls, RA-UIP RA-NSIP demonstrated significantly ability form induce Specifically, exhibited greater capacity myofibroblasts than did patients. Conclusions These findings suggest targeting may be novel therapeutic approach treating RA

Language: Английский

Fibroblasts in rheumatoid arthritis: novel roles in joint inflammation and beyond DOI Creative Commons

Elpida Neofotistou-Themeli,

Panagiota Goutakoli,

Theodoros Chanis

et al.

Frontiers in Medicine, Journal Year: 2025, Volume and Issue: 11

Published: Jan. 21, 2025

High-throughput technologies in human and animal studies have revealed novel molecular cellular pathways involved tissue inflammation of rheumatoid arthritis (RA). Fibroblasts been the forefront research for several decades. Subpopulations with specific phenotypic functional properties characterized both mouse models disease. Data supporting active involvement fibroblasts immune responses remodeling processes, as well their central role promoting clinical relapses contributing to treatment resistance, clearly reshaped disease evolution. The lung is an important non-synovial component RA from a immunopathogenic aspect. Interstitial (ILD) significant contributor burden affecting morbidity mortality. Although our knowledge ILD has progressed, gaps basic science remain, posing hurdles efficient diagnosis, prediction course its effective treatment. contribution this process not defined. focus review on RA-ILD, presenting data genetics associated RA-ILD humans models.

Language: Английский

Citations

0
Neutrophil extracellular traps (NETs) are increased in rheumatoid arthritis-associated interstitial lung disease DOI Creative Commons
Jing Xue,

Miaomiao Nian,

Yangyang Liang

et al.

Respiratory Research, Journal Year: 2025, Volume and Issue: 26(1)

Published: Jan. 22, 2025

Abstract Background Neutrophil extracellular trap (NET) formation has been implicated as a pathogenic mechanism in both rheumatoid arthritis (RA) and interstitial lung disease (ILD). However, the role of NETs RA-associated ILD (RA-ILD) mechanisms driving NET remain unclear. This study aimed to assess involvement RA-ILD elucidate underlying mechanisms. Methods Single-cell sequencing was used identify changes quantity function neutrophils tissue zymosan A (ZYM)-induced pneumonia model. Additionally, nuclear receptor 4A3 (NR4A3) interference performed HL-60 cells its impact on transformation MRC-5 into myofibroblasts. The clinical relevance plasma myeloperoxidase-DNA (MPO-DNA), citrullinated histone 3 (Cit-H3), cell-free DNA evaluated patients with different imaging types via commercial enzyme-linked immunosorbent assay (ELISA). Results In ZYM-treated SKG mouse model, which recapitulates key features RA-ILD, an increased population primarily responsible for formation. Mechanistically, we found that NR4A3 expression enhanced cells, turn promoted differentiation Clinically, MPO-DNA levels are elevated RA-nonspecific (RA-NSIP), whereas Cit-H3 RA-usual (RA-UIP) compared healthy subjects. ROC curve analysis further revealed combination MPO-DNA, factor (RF), anti-citrullinated protein (anti-CCP) Cit-H3, RF, anti-CCP were superior diagnostic panels NSIP UIP patients, respectively. Moreover, those from controls, RA-UIP RA-NSIP demonstrated significantly ability form induce Specifically, exhibited greater capacity myofibroblasts than did patients. Conclusions These findings suggest targeting may be novel therapeutic approach treating RA

Language: Английский

Citations

0