Leucocyte Abnormalities in Synovial Fluid of Degenerative and Inflammatory Arthropathies

Abstract

Genome damage has been related to the induction of autoimmune processes, chronic inflammation, and apoptosis. Recent studies suggest that some rheumatological diseases are associated with overall genomic instability in the T cell compartment. However, no data regarding leucocyte abnormalities in synovial fluid (SF) and their relationship with inflammation are available. The aim of this study was to investigate cellular phenotypes in SF collected from patients with different inflammatory arthropathies, including rhematoid arthritis (RA), psoriatic arthritis (PsA), crystal-induced arthritis (CIA), and non-inflammatory arthropathies, such as osteoarthritis (OA). We found high percentage of micronuclei in SF from CIA compared to the other groups and a high frequency of pyknotic cell in RA and CIA patients. A correlation between pyknosis and immature polymorphonuclear cells with local inflammatory indices was observed. The study of the apoptosis process revealed an increased BAX expression in CIA and RA compared to OA and PsA, while Bcl-2 was higher in CIA. Caspase-3 activity was increased in SF from RA patients and correlates with inflammatory and anti-inflammatory cytokines. In conclusion, our results showed that inflammatory SF is associated with genomic instability and abnormal cell subsets.

Therapeutic potential of Coptis chinensis for arthritis with underlying mechanisms

“…However, the types of arthritis treated with these targets are not completely clear. Targets, β2-adrenergic receptor (ADRB2), AHR, CRP, IRF1, prostaglandin G/H synthase 1 (PTGS1), SPP1 and other targets, exert key effects in the pathogenesis of arthritis, but role of them in the treatment of arthritis with CC has not been confirmed ( Table 3 ) ( Xu et al, 2004 ; Koskela et al, 2012 ; Ko et al, 2013 ; Li et al, 2013 ; Xue et al, 2014 ; Song et al, 2016 ; Trzybulska et al, 2018 ; Bonelli et al, 2019 ; Chu et al, 2019 ; Lin et al, 2019 ; Sun et al, 2020 ; Orecchini et al, 2020 ; Yang et al, 2020 ; Nalesso et al, 2021 ; Tang et al, 2021 ; Xu and Xu, 2021 ; Zou et al, 2021 ; Balasundaram et al, 2022 ; Cai et al, 2022 ; Liu et al, 2022 ; Wang et al, 2022 ; Zhang et al, 2022 ; Zhang et al, 2022 ; Han et al, 2022 ; Man et al, 2022 ; Nguyen et al, 2022 ; Qian et al, 2022 ; Tavallaee et al, 2022 ; Zhuang et al, 2022 ; Afnan et al, 2023 ; Baggio et al, 2023 ; Sun et al, 2023b ; Zhou et al, 2023 ; Fan et al, 2023 ; Huang et al, 2023 ; Ning et al, 2023 ; Qin et al, 2023 ; Skougaard et al, 2023 ; Tu et al, 2023 ; Xie et al, 2023 ; Yan et al, 2023 ; Yu et al, 2023 ; Zhao et al, 2023 ). We have elaborated on the role of targets such as MMP-3, IL-1β, MAPK, IL-6, ADRB2, AHR, CRP, CAV1, CXCL2, SPP1 and other targets in treating arthritis, explored the potential targets and mechanisms of CC in treating arthritis, analyzed the feasibility of CC as an anti-arthritis drug, and provided a theoretical basis for subsequent research.…”

“…However, the types of arthritis treated with these targets are not completely clear. Targets, β2adrenergic receptor (ADRB2), AHR, CRP, IRF1, prostaglandin G/H synthase 1 (PTGS1), SPP1 and other targets, exert key effects in the pathogenesis of arthritis, but role of them in the treatment of arthritis with CC has not been confirmed (Table 3) (Xu et al, 2004;Koskela et al, 2012;Ko et al, 2013;Li et al, 2013;Xue et al, 2014;Song et al, 2016;Trzybulska et al, 2018;Bonelli et al, 2019;Chu et al, 2019;Lin et al, 2019;Sun et al, 2020;Orecchini et al, 2020;Yang et al, 2020;Nalesso et al, 2021;Tang et al, 2021;Zou et al, 2021;Balasundaram et al, 2022;Cai et al, 2022;Liu et al, 2022;Zhang et al, 2022;Zhang et al, 2022;Han et al, 2022;Man et al, 2022;Nguyen et al, 2022;Qian et al, 2022;Tavallaee et al, 2022;Zhuang et al, 2022;Afnan et al, 2023;Baggio et al, 2023;Sun et al, 2023b;Zhou et al, 2023;Fan et al, 2023;Huang et al, 2023;Ning et al, 2023;Qin et al, 2023;Skougaard et al, 2023;Tu et al, 2023;Xie et al, 2023;…”