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Evaluation of the degree of clinical rheumatoid arthritis activity based on the concentrations of cytokines TNF-alpha, IL-12, IL-15, and IL-18 in serum and synovial fluid  [PDF]
Petrovi?-Rackov Ljiljana
Vojnosanitetski Pregled , 2006, DOI: 10.2298/vsp0601021p
Abstract: Bacground/Aim. Experimental in vitro and in vivo investigations in a mouse model have proved that TNF-alpha, IL-12, IL- 15 and IL-18 participate in the pathogenesis of erosive inflammatory arthritis. The aim of this research was to determine the clinical significance of cytokines in the evaluation of the activity of rheumatoid arthritis (RA). Methods. Inside a 4-year period we followed-up 64 patients with RA as newly occurred or in the phase of worsening. We observed the clinical manifestation of the disease upon wluch we divided the patients in to 3 groups: the patients with low active RA, patients with moderate active RA, and the patients with wild active RA. The control group (n = 25 patients) included the patients with osteoarthrosis (OA), and arthritis of the knee. In the samples of serum of all of the patients the concentrating of cytokines TNF-alpha, IL-12, IL-15, and IL-18 were determined using the immunoenzymatic methods in mice for human interleukines. By comparing the concentrations in 30 patients with the high, 14 patients with moderate, and 20 patients with the mild activity of RA it was determined that the patients with the high degree of the disease activity, had significantly high (p < 0.01; p < 0.05) concentrations of the examined cytokines in blood and synovial fluid as compared to the patients with the moderate and mild active disease. There was a relationship (p < 0.01) between the concentrations of cytokines in blood and synovial fluid with the quantity of the Disease Activity Score in 28 joints. Conclusions. Cytokines concentrations could be good indicators of the degree of the general activity of RA. This research could contribute to the interpretation of insufficiently well known views of the pathogenesis role and significance of citokines in an active disease.
Gastrin-releasing peptide, substance P and cytokines in rheumatoid arthritis
Paul G Green
Arthritis Research & Therapy , 2005, DOI: 10.1186/ar1746
Abstract: A lack of a comprehensive understanding of the pathogenesis of rheumatoid arthritis (RA) has hampered the development of novel therapeutic approaches to the treatment of this disease. In the current issue of this journal, Grimsholm and colleagues [1] have investigated a role for neuropeptides in the pathology of RA. Although many different cell types, such as macrophages and synoviocytes, have long been known to be involved in RA, it has recently been realized that the peripheral nervous system has a key role in modulating the severity of RA [2-4]. Synovial tissue is richly innervated with neuropeptide-containing primary afferent and sympathetic neurons [5-7] and there is evidence that the release of these neuropeptides powerfully influences the severity of chronic inflammatory diseases, including RA [8,9]. Grimsholm and colleagues [1] evaluated the relationship between synovial fluid levels of neuropeptides, inflammatory cytokines and duration of disease in patients with RA. Among the five neuropeptides and three cytokines assayed, they observed a significant correlation between the levels of just two neuropeptides, bombesin/gastrin-releasing peptide (BN/GRP) and substance P (SP) with inflammatory cytokines.It is well known that proinflammatory cytokines have a fundamental role in the development and maintenance of RA and other inflammatory diseases. Cytokines such as IL-1, tumor necrosis factor-α (TNF-α) and IL-6 are produced locally in synovial tissue, as well as systemically, where it has been hypothesized they are the principal effectors for the pathological and clinical manifestations of RA [10]. Indeed, several novel therapies that have recently been developed or are currently undergoing clinical trials for RA target several of these cytokines, such as TNF-α (etanercept, adalimumab and infliximab), IL-1 (anakinra) and IL-6 (MRA) [11-14]. However, although there is evidence that anti-cytokine therapies might be effective for patients with RA, it is likely that
Rheumatoid arthritis, gold therapy, contact allergy and blood cytokines
?ke Svensson, Halvor M?ller, Bert Bj?rkner, Magnus Bruze, Ido Leden, Jan Theander, Kjell Ohlsson, Carina Linder
BMC Dermatology , 2002, DOI: 10.1186/1471-5945-2-2
Abstract: Serum cytokines were assayed before and 24 h after the first injection of gold sodium thiomalate (GSTM).Contact allergy to gold was found in 4 of 19 patients. Compared to gold-negative patients (starting dose: 10 mg GSTM), there was a larger increase in serum TNFalpha (p < 0.05), sTNF-R1 (NS), and IL-1 ra (p < 0.05) in gold-allergic patients.Cytokines are released in blood by GSTM in RA patients with gold allergy. To minimize the risk of acute adverse reactions the starting dose of GSTM should be lowered to 5 mg. Alternatively, patients should be patch-tested before gold therapy; in test-positive cases, 5 mg is recommended as the first dose.Contact allergy to gold, as diagnosed by patch testing with gold sodium thiosulfate (GSTS), is very common among patients with eczematous disease [1-3]. These patients are allergic also to other monovalent gold salts such as gold sodium thiomalate (GSTM)[4].We have previously shown that contact allergy to gold is frequent also in rheumatoid arthritis (RA) patients[5]. Furthermore, it has been shown that subjects with a contact allergy to gold experience acute reactions, cutaneous as well as general, if they are exposed parenterally to their contact allergen[6]. The reactions are accompanied by a release of plasma cytokines and acute phase reactants during the first 24 h after the gold injection[7].Gold therapy in RA with GSTM is usually started with a "test dose" of 10 mg to avoid hypersensitivity reactions. In the present study a starting dose of 5 mg was given to patients with a gold allergy while test negative patients obtained the higher standard dose; clinical reactions were registered as well as changes in body temperature and plasma cytokines.The study was performed in 19 patients with RA, 4 males and 15 females, aged 30–75 years, mean age 63.5 years. They all had RA according to the classification criteria of ACR[8] with a median duration of 23 ms (range 4 ms to 20 ys). The patients were selected because of a planned trea
Differential activation of JAK enzymes in rheumatoid arthritis and autoimmune disorders by pro-inflammatory cytokines: potential drug targets
Charles J Malemud
International Journal of Interferon, Cytokine and Mediator Research , 2010, DOI: http://dx.doi.org/10.2147/IJICMR.S9470
Abstract: ential activation of JAK enzymes in rheumatoid arthritis and autoimmune disorders by pro-inflammatory cytokines: potential drug targets Review (4806) Total Article Views Authors: Charles J Malemud Published Date October 2010 Volume 2010:2 Pages 97 - 111 DOI: http://dx.doi.org/10.2147/IJICMR.S9470 Charles J Malemud Arthritis Research Laboratory, Division of Rheumatic Diseases, Department of Medicine, Case Western Reserve University School of Medicine, Cleveland, OH, USA Abstract: Although several pro-inflammatory cytokines including interleukin-6 (IL-6), IL-7, IL-12/IL-23, IL-17, IL-2, interferon, and the anti-inflammatory cytokines, IL-4/IL-13, IL-10, and IL-22, all activate the Janus kinase/signal transducers and activators of transcription (JAK/STAT) pathway, in autoimmune disorders, a skewing of the cytokine repertoire in favor of pro-inflammatory cytokines results in amplifying the effects of pro-inflammatory cytokines. An apparent deficiency of anti-inflammatory cytokines to counterbalance the ‘ramping up’ of pro-inflammatory cytokine-mediated activation of JAK/STAT is also significant, while endogenous negative regulators of cytokine signaling and JAK/STAT activation may also be compromised. In addition, JAK/STAT pathway activation can result in activation of stress-activated protein/mitogen-activated protein kinase (SAP/MAPK) and phosphatidylinositol-3-kinase/Akt/mammalian target of rapamycin pathways that are instrumental in promoting matrix metalloproteinase gene expression, aberrant cell survival, and osteoclast differentiation. The critical role played by pro-inflammatory cytokines in differentially activating JAK/STAT and parallel signal transduction pathways resulted in the development of several cytokine/cytokine receptor neutralizing monoclonal antibodies and fusion proteins that are currently employed for treating rheumatoid arthritis, Crohn’s disease, and psoriasis. Small molecule inhibitors (SMIs) that target specific JAK enzymes have led to the development of CP690550, a JAK3-specific SMI, which is the first JAK-specific SMI to reach phase III in a rheumatoid arthritis clinical trial.
Supplementation of diet with krill oil protects against experimental rheumatoid arthritis
Michelle Ierna, Alison Kerr, Hannah Scales, Kjetil Berge, Mikko Griinari
BMC Musculoskeletal Disorders , 2010, DOI: 10.1186/1471-2474-11-136
Abstract: Collagen-induced arthritis susceptible DBA/1 mice were provided ad libitum access to a control diet or diets supplemented with either krill oil or fish oil throughout the study. There were 14 mice in each of the 3 treatment groups. The level of EPA + DHA was 0.44 g/100 g in the krill oil diet and 0.47 g/100 g in the fish oil diet. Severity of arthritis was determined using a clinical scoring system. Arthritis joints were analysed by histopathology and graded. Serum samples were obtained at the end of the study and the levels of IL-1α, IL-1β, IL-7, IL-10, IL-12p70, IL-13, IL-15, IL-17 and TGF-β were determined by a Luminex? assay system.Consumption of krill oil and supplemented diet significantly reduced the arthritis scores and hind paw swelling when compared to a control diet not supplemented with EPA and DHA. However, the arthritis score during the late phase of the study was only significantly reduced after krill oil administration. Furthermore, mice fed the krill oil diet demonstrated lower infiltration of inflammatory cells into the joint and synovial layer hyperplasia, when compared to control. Inclusion of fish oil and krill oil in the diets led to a significant reduction in hyperplasia and total histology score. Krill oil did not modulate the levels of serum cytokines whereas consumption of fish oil increased the levels of IL-1α and IL-13.The study suggests that krill oil may be a useful intervention strategy against the clinical and histopathological signs of inflammatory arthritis.Arthritis and musculoskeletal disorders are among the most prevalent chronic conditions affecting the US population [1]. Osteoarthritis, also known as osteoarthrosis or degenerative joint disease, is the most common type of arthritis, characterised primarily by cartilage loss and synovitis as a result of the aging process and affects approximately 12.1% of the US population aged 25 years or older [1,2]. Similarly, rheumatoid arthritis (RA) is a major cause of morbidity in the Wes
Effect of bizhongxiao decotion (BZXD) on some cytokines in plasma of rats with CⅡ-induced rheumatoid arthritis
WANG An-yu,LIANG Qing-hua,Luo-xu,BAO Tai-cheng
International Journal of Biomedical Science , 2005,
Abstract: Objective: To investigate the influence of bizhongxiao decoction(BZXD) which is a Traditional Chinese medicine for RA including, on the plasma TNF-α and IL-1β in rats with CⅡ-induced arthritis (CIA) and explore the protective mechanism of BZXD in the treatment of rheumatoid arthritis . Methods: 75 SD rats were divided into four groups randomly. Normal control group (n=5) not be treated any more. The CIA rat was established by subcutaneous injection with bovine Ⅱ collagen(BⅡC) and complete Freund,s adjuvant(CFA) after 7d breeding. The CIA rats were divided into the CIA group(n=16)、BZXD group (n=29) treated with BZXD and the MTX group(n=25) treated with methotrexate. All rats were killed after various intervals(25,30,35,40,or 45d). At the end of each time interval, we collected the blood of each rat. To detect TNF-αand IL-1βin plasma with radio-immunity kit. Results: BⅡC and CFA can be used to copying CIA model. The incidence of arthritis was 88%. The plasma TNF-αand IL-1βlevels of CIA group, BZXD group and MTX group were notably higher than those of normal control group(p<0.05), moreover, the CIA group was higher than those of the MTX group and BZXD group at various interval (p<0.01). TNF-αand IL-1βrose step by step in CIA group but decreased in BZXD group and MTX group gradually. Moreover, in BZXD group were lower than those in MTX group (p<0.05). Conclusion: TNF-αand IL-1βplay a very important role in the formation and development of RA. BZXD can notably decrease the plasma TNF-αand IL-1βlevels, which was better than MTX. Key words: bizhongxiao decotion, methotrexate, arthritis, rheumatoid, TNF-α, IL-1β Rheumatoid arthritis (RA) is particular with chronic and symmetric arthritis which get along with joint damage and matrix erosion. But its mechanism has not been clear. The recent research has demonstrated that TNF - α and IL-1β play key role in the disease of RA and made progress with matrix erosion. To explore the mechanism of the RA and the function of BZXD ,we make the collagen-induced arthritis rat and treated with BZXD, then detect the level of TNF-αand IL-1βin plasma at various interval.
Critical Involvement of Cytokines and Chemokines in the Pathogenesis of Rheumatoid Vasculitis
Tsuyoshi Kasama, Takeo Isozaki, Kuninobu Wakabayashi, Tsuyoshi Odai and Mizuho Matsunawa
Clinical Medicine Insights: Arthritis and Musculoskeletal Disorders , 2012,
Abstract: Vasculitis in rheumatoid arthritis (rheumatoid vasculitis) has a heterogeneous clinical presentation that includes skin disorders, neuropathy, eye symptoms and systemic inflammation. The molecular mechanisms underlying rheumatoid vasculitis are not fully understood; however, the importance of a chronic imbalance of the cytokines and chemokines involved in orchestrating infl ammatory responses is well established in patients with rheumatoid arthritis, and similar dysregulation of these mediators has been suggested to occur in patients with rheumatoid vasculitis. In the present review, we discuss the involvement of cytokines and chemokines in the pathogenesis of rheumatoid vasculitis and evaluate their utility as laboratory parameters of active vasculitic disease. Also the involvement of adhesion molecules is discussed.
Critical Involvement of Cytokines and Chemokines in the Pathogenesis of Rheumatoid Vasculitis
Tsuyoshi Kasama,Takeo Isozaki,Kuninobu Wakabayashi,Tsuyoshi Odai and Mizuho Matsunawa
Clinical Medicine : Arthritis and Musculoskeletal Disorders , 2008,
Abstract: Vasculitis in rheumatoid arthritis (rheumatoid vasculitis) has a heterogeneous clinical presentation that includes skin disorders, neuropathy, eye symptoms and systemic inflammation. The molecular mechanisms underlying rheumatoid vasculitis are not fully understood; however, the importance of a chronic imbalance of the cytokines and chemokines involved in orchestrating infl ammatory responses is well established in patients with rheumatoid arthritis, and similar dysregulation of these mediators has been suggested to occur in patients with rheumatoid vasculitis. In the present review, we discuss the involvement of cytokines and chemokines in the pathogenesis of rheumatoid vasculitis and evaluate their utility as laboratory parameters of active vasculitic disease. Also the involvement of adhesion molecules is discussed.
Levels of gastrin-releasing peptide and substance P in synovial fluid and serum correlate with levels of cytokines in rheumatoid arthritis
Ola Grimsholm, Solbritt Rantap??-Dahlqvist, Sture Forsgren
Arthritis Research & Therapy , 2005, DOI: 10.1186/ar1503
Abstract: It has long been known that neuropeptides are secreted locally during immune responses [1], and that they are involved in vasodilation and plasma extravasation, that is, neurogenic inflammation [2,3]. It is furthermore known that inflammatory cells can produce neuropeptides [4,5]. The neuropeptide substance P (SP) has been extensively examined in normal joints and in rheumatoid arthritis (RA) during the past two decades. SP has known proinflammatory properties, enhancing the proliferation of rheumatoid synoviocytes [6] and inducing the release of the proinflammatory mediator prostaglandin E2 and destructive enzymes such as collagenase [6]. An increased level of SP has been observed in the synovial fluid from RA patients [7-11].Another neuropeptide is gastrin-releasing peptide (GRP) [12], the mammalian homologue of bombesin (BN), a tetradecapeptide originally isolated from the skin of the frog Bombina bombina [13]. BN/GRP-like peptides affect several systems in mammals, such as satiety, thermal regulation, nociception, and the activation of the sympatho-adrenomedullary outflow [14,15]. We have recently shown that BN/GRP-like peptides are present in joint fluid in arthritis and that they are increased in amount in RA [11]. Several other neuropeptides, such as vasoactive intestinal peptide (VIP), calcitonin-gene-related peptide (CGRP), and neuropeptide Y (NPY), have also been found in synovial fluid from patients with RA [10,16]. VIP is a potent anti-inflammatory agent [17,18]. It therefore has a beneficial effect in collagen-induced arthritis (CIA) [17], inhibits the production of proinflammatory factors, including tumour necrosis factor (TNF)-α [19,20] and chemokines [21], and inhibits IL-2 production in stimulated murine T lymphocytes [22].The proinflammatory cytokine TNF-α plays a central role in the pathogenesis of RA [23,24]. Increased concentrations of this cytokine in synovial fluid from RA patients have been reported in several studies (e.g. [25-27]). It has a
Bifocal Distraction in Patient with Rheumatoid Arthritis and Severe Condylar Degeneration: Report of Case
Chaves Neto,Henrique Duque de Miranda; Olate,Sergio; Mazzonetto,Renato; Spagnoli,Daniel B;
International Journal of Morphology , 2011, DOI: 10.4067/S0717-95022011000100033
Abstract: facial involvement in patients with rheumatoid arthritis is variable depending on the type, onset, and duration of the disease. the treatment of patients with open bite resulting from degenerative changes on the condyles can be a challenge for the surgeon. rheumatoid arthritis is a systemic disorder of unknown etiology characterized by chronic inflammation and proliferation of synovial tissue. studies showed that patients with rheumatoid arthritis can developed progressive osteoarthrosis that result in gross radiographic changes in the condyles. with the development of distraction osteogénesis for treatment of mandible hypoplasia a new chapter has been opened in the surgical management of patients with rheumatoid arthritis associated with skeletal deficiency. the aim of this paper is to evaluate osteogenesis distraction for treatment of anterior open bite in patients with rheumatoid arthritis and severe condylar degeneration.
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