scholarly journals STAT3 is critical to promote inflammatory cytokines and RANKL expression in inflammatory arthritis

2012 ◽  
Vol 14 (S1) ◽  
Author(s):  
Takeshi Miyamoto ◽  
Tomoaki Mori ◽  
Akihiko Yoshimura ◽  
Toshiaki Toyama
Keyword(s):  
Inflammatory Cytokines ◽  
Inflammatory Arthritis ◽  
Rankl Expression

scholarly journals IL-1  and TNF -initiated IL-6-STAT3 pathway is critical in mediating inflammatory cytokines and RANKL expression in inflammatory arthritis

2011 ◽  
Vol 23 (11) ◽  
pp. 701-712 ◽  
Author(s):  
T. Mori ◽  
T. Miyamoto ◽  
H. Yoshida ◽  
M. Asakawa ◽  
M. Kawasumi ◽  
...  
Keyword(s):  
Inflammatory Cytokines ◽  
Inflammatory Arthritis ◽  
Rankl Expression ◽  
Stat3 Pathway

Cannabidiol decreases bone resorption by inhibiting RANK/RANKL expression and pro-inflammatory cytokines during experimental periodontitis in rats

2009 ◽  
Vol 9 (2) ◽  
pp. 216-222 ◽  
Author(s):  
Marcelo H. Napimoga ◽  
Bruno B. Benatti ◽  
Flavia O. Lima ◽  
Polyanna M. Alves ◽  
Alline C. Campos ◽  
...  
Keyword(s):  
Bone Resorption ◽  
Inflammatory Cytokines ◽  
Rankl Expression ◽  
Experimental Periodontitis ◽  
Pro Inflammatory Cytokines

scholarly journals Critical Roles for Interleukin 1 and Tumor Necrosis Factor α in Antibody-induced Arthritis

2002 ◽  
Vol 196 (1) ◽  
pp. 77-85 ◽  
Author(s):  
Hong Ji ◽  
Allison Pettit ◽  
Koichiro Ohmura ◽  
Adriana Ortiz-Lopez ◽  
Veronique Duchatelle ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Tumor Necrosis Factor ◽  
Inflammatory Cytokines ◽  
Inflammatory Arthritis ◽  
Tumor Necrosis ◽  
Environmental Changes ◽  
Bone Erosion ◽  
Bone Destruction ◽  
Tnf Α ◽  
Necrosis Factor

In spontaneous inflammatory arthritis of K/BxN T cell receptor transgenic mice, the effector phase of the disease is provoked by binding of immunoglobulins (Igs) to joint surfaces. Inflammatory cytokines are known to be involved in human inflammatory arthritis, in particular rheumatoid arthritis, although, overall, the pathogenetic mechanisms of the human affliction remain unclear. To explore the analogy between the K/BxN model and human patients, we assessed the role and relative importance of inflammatory cytokines in K/BxN joint inflammation by transferring arthritogenic serum into a panel of genetically deficient recipients. Interleukin (IL)-1 proved absolutely necessary. Tumor necrosis factor (TNF)–α was also required, although seemingly less critically than IL-1, because a proportion of TNF-α–deficient mice developed robust disease. There was no evidence for an important role for IL-6. Bone destruction and reconstruction were also examined. We found that all mice with strong inflammation exhibited the bone erosion and reconstruction phenomena typical of K/BxN arthritis, with no evidence of any particular requirement for TNFα for bone destruction. The variability in the requirement for TNF-α, reminiscent of that observed in treated rheumatoid arthritis patients, did not appear genetically programmed but related instead to subtle environmental changes.

scholarly journals Intraarticular corticosteroids decrease synovial RANKL expression in inflammatory arthritis

2006 ◽  
Vol 54 (5) ◽  
pp. 1463-1472 ◽  
Author(s):  
Dimitrios Makrygiannakis ◽  
Erik af Klint ◽  
Sergiu-Bogdan Catrina ◽  
Ileana Ruxandra Botusan ◽  
Elin Klareskog ◽  
...  
Keyword(s):  
Inflammatory Arthritis ◽  
Rankl Expression ◽  
Intraarticular Corticosteroids

scholarly journals AB0057 THE ROLE OF NON-INFLAMMATORY MACROPHAGES INITIATING AND RESOLVING THE INFLAMMATORY RESPONSE OF MONOSODIUM URATE IN MICE

2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 1330.1-1331
Author(s):  
Y. J. Huang ◽  
L. C. Wang ◽  
C. F. Kuo
Keyword(s):  
Inflammatory Response ◽  
Inflammatory Cytokines ◽  
Inflammatory Arthritis ◽  
Protein Production ◽  
Gouty Arthritis ◽  
Acute Gouty Arthritis ◽  
Tnf Α ◽  
The World ◽  
Inflammatory Macrophages ◽  
Msu Crystals

Background:Gout is the most common chronic inflammatory arthritis around the world which is associated with many conditions that affect longevity and well-being, such as metabolic syndrome, cardiovascular diseases, and renal diseases. [1]Objectives:Gout is the most common inflammatory arthritis around the world. Innate immunity has been implicated in gout inflammation in recent years. However, the phenomena of maintenance of ‘asymptomatic’ hyperuricemia, the spontaneous resolution of acute gouty arthritis and non-inflammatory tophus and its association with immune regulation are still elusive. We propose that resident macrophages may be a key player in the suppression of gouty inflammation. To address this hypothesis, we used non-inflammatory macrophages to explore the role played in initiating or resolving the inflammatory response.Methods:Bone marrow-derived macrophages (BMDM) were stimulated with monosodium rate (MSU), then analyzed the expression of RNA and protein of inflammatory cytokines, including IL-1β, IL-18 and TNF-α. In addition, we also observe the ability of macrophage to phagocyte and hydrolyze MSU crystal.Results:Our results indicate that MSU alone could not induce IL-1β, IL-18, and TNF-α mRNA expression and protein production. However, when macrophages were pre-stimulated with lipopolysaccharide (LPS) or MSU, as well as in combination the production of IL-1β and IL-18 were significantly increased. Furthermore, MSU maybe amplifies LPS-induced protein production of IL-1β and IL-18 but not in TNF-α. A temporal delay in the correlation between mRNA expression and protein production was shown. The results also indicated that macrophages could not only phagocytize MSU crystals but may also hydrolyze MSU crystals.Conclusion:These data indicate that MSU crystal alone is insufficient to induce pro-inflammatory cytokines production, however, when exposed to an infectious source of infection, it will amplify the inflammatory response and there is a synergistic effect between MSU and LPS. This may explain the diverse clinic phenomena of ‘asymptomatic’ hyperuricemia, non-inflammatory tophus and acute gouty arthritis. The high efficiency of phagocytosis and hydrolyzed MSU crystals of macrophages may explain the spontaneous regression of acute gouty arthritis. These findings may provide a new therapy for the prevention and treatment of acute gout attacks.References:[1]Kuo CF, Grainge MJ, Mallen C, Zhang W, Doherty M. Comorbidities in patients with gout prior to and following diagnosis: case-control study. Annals of the rheumatic diseases. 2014 Nov 14.Disclosure of Interests:None declared

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