scholarly journals Cinnamic Aldehyde, the main monomer component of Cinnamon , exhibits anti‐inflammatory property in OA synovial fibroblasts via TLR4/MyD88 pathway

2021 ◽  
Author(s):  
Pu Chen ◽  
Jun Zhou ◽  
Anmin Ruan ◽  
Lingfeng Zeng ◽  
Jun Liu ◽  
...  
Keyword(s):  
Synovial Fibroblasts ◽  
Cinnamic Aldehyde ◽  
Anti Inflammatory ◽  
Myd88 Pathway

scholarly journals The activin-follistatin anti-inflammatory cycle is deregulated in synovial fibroblasts

2019 ◽  
Vol 21 (1) ◽  
Author(s):  
Magnus Diller ◽  
Klaus Frommer ◽  
Berno Dankbar ◽  
Ingo Tarner ◽  
Marie-Lisa Hülser ◽  
...  
Keyword(s):  
Synovial Fibroblasts ◽  
Anti Inflammatory

scholarly journals AB0043 EFFECT OF ANTI-INFLAMMATORY MEDICATION ON INTERACTION OF SYNOVIAL FIBROBLASTS WITH MACROPHAGES IN RHEUMATOID ARTHRITIS

2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 1054.1-1054
Author(s):  
M. Schmeller ◽  
M. Diller ◽  
R. Hasseli ◽  
A. Knothe ◽  
S. Rehart ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Mononuclear Cells ◽  
Joint Inflammation ◽  
Synovial Fibroblasts ◽  
Therapeutic Effects ◽  
Synergistic Activity ◽  
M1 Macrophages ◽  
Healthy Donors ◽  
Proinflammatory Activity ◽  
Anti Inflammatory

Background:One of the key mechanisms in the pathogenesis of rheumatoid arthritis (RA) is the interaction of macrophages and synovial fibroblasts during joint inflammation. Increased synergistic proinflammatory activity of both cell types leads to the release of high levels of proinflammatory cytokines, especially of interleukin-6 (IL-6), and of matrix degrading enzymes. If this mechanism is uncontrolled, progressive destruction of articular cartilage and bone will take place.In active disease, immediate anti-inflammatory treatment with glucocorticoids is usually replaced by disease-modifying anti-rheumatic drugs (DMARDS), especially by methotrexate (MTX) and biologics such as TNF-α- or IL-6-inhibitors. This led to great improvements in prognosis and outcome for RA patients. However, about 40% of patients experience no remission or suffer from side effects of medication. To optimize established substances and to develop new treatment strategies, it is necessary to understand the mechanisms underlying the limited therapeutic effects.Objectives:Evaluation of the effect of prednisolone, MTX, adalimumab, tocilizumab on IL-6 secretion by RA synovial fibroblasts (RASF) and macrophages.Methods:RA synovium was used for RASF isolation. Peripheral blood mononuclear cells (PBMCs) were isolated from blood of healthy donors and RA patients by using Ficoll© medium followed by density gradient centrifugation. Mononuclear cells were seeded on six well plates (6x10^6/well) and incubated for one week. Then they were stimulated with Interferon-у (20 ng/ml) and LPS (50 ng/ml) for 48h to initiate differentiation into proinflammatory M1 macrophages. The M1 macrophages were co-cultured with RASF (100.000/well) and different treatments added (prednisolone: 10, 25, 50, 75, 100 nM, 1 µM; adalimumab: 100, 500 µg/ml; tocilizumab: 1, 5 µg/ml; MTX: 0,5, 1, 5, 10, 100 nM, 1µM). After 24h culture supernatants were collected and IL-6- and TNFα-ELISAs were performed.Results:IL-6 concentrations of untreated controls were comparable, regardless whether M1 macrophages from healthy donors or RA-patients were used for co-culture. Prednisolone reduced co-culture-induced IL-6 up to 56% (p<0.001) in co-culture of RASF and M1 macrophages of healthy donors and up to 60% (p<0.001) in co-culture of RASF and RA M1 macrophages. Adalimumab reduced IL-6 up to 28% (p<0.05) in M1 of healthy donors and up to 45% (p<0.01) in RA M1 macrophage co-cultures. A minor reduction by 10-20% of IL-6 was observed with tocilizumab and no significant effect could be achieved after treatment with MTX.Conclusion:Prednisolone and adalimumab clearly decrease but do not eliminate proinflammatory synergistic activity of RASF and M1 macrophages. These results confirm the clinical observation, that there is a large number of RA-patients that independent of anti-inflammatory treatment still suffer from low-level joint inflammation.The synergistic proinflammatory activity of M1 macrophages and RASF seems to be a complex and multifactorial mechanism that is difficult to eliminate by a single treatment substance. Since it is one of the key mechanisms in RA pathogenesis, there is a critical need to investigate how therapy effects could be optimized. This study confirmed RASFs as one of the leading effector cells of increased synergistic proinflammatory activity, thus underlining their promising role as a treatment target in rheumatoid arthritis.Disclosure of Interests:None declared

Anti-inflammatory effects of ursolic acid-3-acetate on human synovial fibroblasts and a murine model of rheumatoid arthritis

2017 ◽  
Vol 49 ◽  
pp. 118-125 ◽  
Author(s):  
Jong Yeong Lee ◽  
Jin Kyeong Choi ◽  
Na-Hee Jeong ◽  
Jeongsoo Yoo ◽  
Yeong Su Ha ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Ursolic Acid ◽  
Murine Model ◽  
Synovial Fibroblasts ◽  
Anti Inflammatory

scholarly journals Polyene Phosphatidylcholine Interacting with TLR-2 Prevents the Synovial Inflammation via Inactivation of MAPK and NF-κB Pathways

2021 ◽  
Author(s):  
Zixuan Xu ◽  
Wenting Hao ◽  
Daxiang Xu ◽  
Yan He ◽  
Ziyi Yan ◽  
...  
Keyword(s):  
Inflammatory Cytokines ◽  
Ex Vivo ◽  
Mapk Pathway ◽  
Synovial Fibroblasts ◽  
Underlying Mechanism ◽  
Inhibitory Effect ◽  
Synovial Inflammation ◽  
Joint Disease ◽  
Drug Candidate ◽  
Anti Inflammatory

Abstract Rheumatoid arthritis (RA) is a chronic autoimmune joint disease that causes cartilage and bone damage or even disability, seriously endangering human health. Chronic synovial inflammation has been shown to play a vital role in the disease sustainability. Therefore, down-regulation of synovial inflammation is considered to be an effective discipline for RA therapy. Polyene phosphatidylcholine (PPC) is a hepatoprotective agent, which was observed to inhibit inflammation in macrophages and prevent collagen-induced arthritis (CIA) of rats in our previous study. However, the underlying mechanism remains unclear. The present study further reported that PPC can inhibit the synovial inflammation. In lipopolysaccharide (LPS)-stimulated primary synovial fibroblasts (SFs) of mice, PPC significantly decreased pro-inflammatory cytokines production while increasing anti-inflammatory cytokines level. In this process, PPC down-regulated the expression of TLR-2 and their downstream signaling molecules such as MyD88, p-ERK1/2, p-JNK1/2, p-P38 in the MAPK pathway and p-IκBα and NF-κB-p65 in NF-kB pathway. Moreover, the inhibitory effect of PPC on the above molecules and cytokines was weakened after the use of TLR-2 agonist Pam3CSK4. However, PPC lost its anti-inflammatory effect and showed an activation of MAPK and NF-kB pathways in the TLR-2-/- primary SFs after exposure to LPS. Furthermore, these results were confirmed in the SFs from the CIA mouse ex vivo. Collectively, this study demonstrated that PPC can alleviate synovial inflammation through TLR-2 mediated MAPK and NF-κB pathways, which can be proposed to be a potential drug candidate for RA therapy.

scholarly journals Clinical Trial andIn VitroStudy for the Role of Cartilage and Synovia in Acute Articular Infection

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Elia R. Langenmair ◽  
Eva J. Kubosch ◽  
Gian M. Salzmann ◽  
Samuel Beck ◽  
Hagen Schmal
Keyword(s):  
Clinical Trial ◽  
Cell Function ◽  
Joint Infection ◽  
Synovial Fibroblasts ◽  
Joint Infections ◽  
Anti Inflammatory

Objective. Osteoarthritis is a long-term complication of acute articular infections. However, the roles of cartilage and synovia in this process are not yet fully understood.Methods. Patients with acute joint infections were enrolled in a prospective clinical trial and the cytokine composition of effusions compared in patients with arthroplasty (n= 8) or with intact joints (n= 67). Cytokines and cell function were also analyzed using a humanin vitromodel of joint infection.Results. Synovial IL-1βlevels were significantly higher in patients with arthroplasty (p= 0.004). Higher IL-1βconcentrations were also found in thein vitromodel without chondrocytes (p< 0.05). The anti-inflammatory cytokines IL-4 and IL-10 were consistently expressedin vivoandin vitro, showing no association with the presence of cartilage or chondrocytes. In contrast, FasL levels increased steadilyin vitro, reaching higher levels without chondrocytes (p< 0.05). Likewise, the viability of synovial fibroblasts (SFB) during infection was higher in the presence of chondrocytes. The cartilage-metabolism markers aggrecan and bFGF were at higher concentrations in intact joints, but also synthesized by SFB.Conclusions. Our data suggest an anti-inflammatory effect of cartilage associated with the SFBs’ increased resistance to infections, which displayed the ability to effectively synthesize cartilage metabolites.The trial is registered with DRKS00003536, MISSinG.

scholarly journals Release kinetic of pro- and anti-inflammatory biomolecules from platelet-rich plasma and functional study on osteoarthritis synovial fibroblasts

Cytotherapy ◽  
2020 ◽  
Vol 22 (7) ◽  
pp. 344-353 ◽  
Author(s):  
Erminia Mariani ◽  
Alice Roffi ◽  
Luca Cattini ◽  
Lia Pulsatelli ◽  
Elisa Assirelli ◽  
...  
Keyword(s):  
Platelet Rich Plasma ◽  
Synovial Fibroblasts ◽  
Functional Study ◽  
Release Kinetic ◽  
Anti Inflammatory

Ursolic acid exhibits anti-inflammatory effects through blocking TLR4-MyD88 pathway mediated by autophagy

Cytokine ◽  
2019 ◽  
Vol 123 ◽  
pp. 154726 ◽  
Author(s):  
Jun Zhao ◽  
Haoyi Zheng ◽  
Zhongguo Sui ◽  
Fanbo Jing ◽  
Xianghua Quan ◽  
...  
Keyword(s):  
Ursolic Acid ◽  
Anti Inflammatory ◽  
Myd88 Pathway
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