Correlation of Plasma Interleukin 1 Levels With Disease Activity in Rheumatoid Arthritis

Eastgate, JulieA; Wood, N. C.; Giovine, FrancescoS Di; Symons, J. A.; Grinlinton, F. M.; Duff, G. W.

doi:10.1016/s0140-6736(88)90185-7

Cited by 450 publications

(195 citation statements)

References 19 publications

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“…Tumour necrosis factor (TNF), interleukin-1 (IL-1), and IL-6 are clearly involved in the arthritic process since all three cytokines are present in synovial¯uid and can be detected immunohistochemically in the in¯amed rheumatoid synovium (Delauran et al, 1992;Farahat et al, 1993). Furthermore, both local and systemic levels of each cytokine correspond to disease activity (Eastgate et al, 1988;Westacott et al, 1990;Feldmann et al, 1990), and TNF and IL-1 have profound catabolic e ects on articular cartilage explants from numerous species (Dingle et al, 1987a;Shinmei et al, 1989).…”

Section: Introductionmentioning

confidence: 99%

RETRACTED: Cloricromene, a coumarine derivative, protects against collagen‐induced arthritis in Lewis rats

Cuzzocrea

Mazzon

Bevilaqua

et al. 2000

British J Pharmacology

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1 The aim of the present study was to investigate the e ects of cloricromene, a coumarine derivative, in rats subjected to collagen-induced arthritis. 2 Collagen-induced arthritis (CIA) was induced in Lewis rats by an intradermal injection of 100 ml of the emulsion (containing 100 mg of bovine type II collagen) (CII) and complete Freund's adjuvant (CFA) at the base of the tail. On day 21, a second injection of CII in CFA was administered. 3 Lewis rats developed an erosive hind paw arthritis when immunized with CII in CFA. Macroscopic clinical evidence of CIA ®rst appeared as peri-articular erythema and oedema in the hind paws. The incidence of CIA was 100% by day 27 in the CII challenged rats and the severity of CIA progressed over a 35-day period with radiographic evaluation revealing focal resorption of bone together with osteophyte formation in the tibiotarsal joint and soft tissue swelling. 4 The histopathology of CIA included erosion of the cartilage at the joint margins. Treatment of rats with cloricromene (10 mg kg 71 i.p. daily) starting at the onset of arthritis (day 23), delayed the development of the clinical signs at days 24 ± 35 and improved histological status in the knee and paw. 5 Immunohistochemical analysis for iNOS, COX-2, nitrotyrosine and for poly (ADP-ribose) synthetase (PARS) revealed a positive staining in in¯amed joints from collagen-treated rats. The degree of staining for iNOS, COX-2, nitrotyrosine and PARS were markedly reduced in tissue sections obtained from collagen-treated rats, which had received cloricromene. 6 Radiographic signs of protection against bone resorption and osteophyte formation were present in the joints of cloricromene-treated rat. 7 This study provides the ®rst evidence that cloricromene, a coumarine derivative, attenuates the degree of chronic in¯ammation and tissue damage associated with collagen-induced arthritis in the rat.

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Section: Introductionmentioning

confidence: 99%

RETRACTED: Cloricromene, a coumarine derivative, protects against collagen‐induced arthritis in Lewis rats

Cuzzocrea

Mazzon

Bevilaqua

et al. 2000

British J Pharmacology

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“…The observation that high levels of disease activity constitutes an independent risk factor for systemic osteoporosis in RA (8,(13)(14)(15) has fed the assumption that inflammation per se contributes importantly to the loss of bone. This hypothesis is supported by several observations: first, proinflammatory cytokines, such as TNF␣, IL-1, and IL-6, are found to be systemically up-regulated in RA patients (41)(42)(43). Second, proinflammatory cytokines such as TNF and IL-1 induce a molecule that is pivotally involved in the activation and differentiation of osteoclasts; that molecule is RANKL, which engages its receptor RANK on osteoclast precursor cells (24)(25)(26)(27).…”

Section: Discussionmentioning

confidence: 80%

Osteoprotegerin protects against generalized bone loss in tumor necrosis factor–transgenic mice

Schett¹,

Redlich²,

Hayer³

et al. 2003

Arthritis & Rheumatism

139

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Objective. To investigate the role of tumor necrosis factor (TNF) in systemic bone loss of chronic inflammatory conditions, such as rheumatoid arthritis (RA), and to address the therapeutic potential of osteoclast blockade.Methods. We investigated systemic bone changes in human TNF transgenic (hTNFtg) mice, which spontaneously developed severe inflammatory arthritis.Results. Osteodensitometry revealed a significant decrease in trabecular bone mineral density (BMD) (؊37%) in hTNFtg mice, and histomorphometry revealed a dramatic loss of bone volume (؊85%) compared with wild-type controls. Osteoclast-covered bone surface and serum levels of deoxypyridinoline crosslinks were significantly elevated, suggesting increased osteoclast-mediated bone resorption in hTNFtg mice. Osteoprotegerin (OPG) completely blocked TNFmediated bone loss by increasing BMD (؉89%) and bone volume (؉647%). Most strikingly, formation of primary spongiosa was dramatically increased (؉563%) in hTNFtg mice after OPG treatment. Osteoclastcovered bone surface and serum levels of deoxypyridinoline crosslinks were significantly decreased by OPG, suggesting effective blockade of osteoclast-mediated bone resorption. OPG did not influence levels of hTNF, TNF receptor I (TNFRI), interleukin-1␤ (IL-1␤), and IL-6. However, OPG decreased bone formation parameters (osteoblast-covered bone surface and serum osteocalcin levels), which were elevated in hTNFtg mice. In contrast to OPG, bisphosphonates and anti-TNF treatment did not affect generalized bone loss in hTNFtg mice. Anti-TNF, however, did not affect levels of TNF and TNFRI at the concentrations tested. These data indicate that generalized bone loss due to increased TNF can be blocked by OPG.Conclusion. OPG may represent a potent tool for preventing generalized loss of bone mass in chronic inflammatory disorders, especially RA.

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“…MMP-2, MMP-3, MMP-9, and MMP-13 are all active in RA (47) and contribute to osteoclast-induced bone resorption (49). Furthermore, these 4 MMPs are induced by IL-1␤, IL-6, TNF␣, and transforming growth factor ␤ (TGF␤), all of which are also implicated in RA (48,50,51) and can be secreted by fibrocytes. Type II collagen is the primary collagen in articular cartilage and is preferentially degraded by MMP-13 (48).…”

Section: Discussionmentioning

confidence: 99%

Circulating fibrocytes contribute to the pathogenesis of collagen antibody–induced arthritis

Galligan¹,

Fish²

2012

Arthritis & Rheumatism

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Objective. Rheumatoid arthritis (RA) is a systemic autoimmune disease resulting in joint inflammation. Fibroblast-like synoviocytes in affected joints are responsible for pannus formation and cytokine/ chemokine production, resulting in leukocyte recruitment and bone/cartilage destruction. Previously, we identified a multipotent stem cell population of activated fibrocytes in the blood of patients with RA that may have a role in disease pathogenesis, perhaps as fibroblast-like synoviocyte precursors. The aim of this study was to further characterize the contribution of circulating fibrocytes to the pathogenesis of RA.Methods. Circulating fibrocytes were isolated from mice with collagen-induced arthritis and transferred intravenously into recipient mice with collagen antibody-induced arthritis (CAIA). The activation status of circulating fibrocytes was determined using multidimensional phosphoflow cytometric analysis of the signaling effectors STAT-5, STAT-1, AKT, and JNK. Circulating fibrocyte trafficking and matrix metalloproteinase (MMP) activity were assessed in real time using fluorescence molecular tomography, specifically labeling circulating fibrocytes with CellVue Maroon and measuring MMP activity using MMPSense 680.Results. The numbers of circulating fibrocytes were increased early during the onset of CAIA, concomitant with their activation, as measured by phosphorylation of STAT-5. Adoptive transfer of circulating fibrocytes augmented disease scores and increased class II major histocompatibility complex expression and peripheral blood phosphoactivation profiles in recipient mice with CAIA. Notably, adoptively transferred fluorescence-labeled circulating fibrocytes rapidly migrated into the affected joints of recipient mice with CAIA, and this was associated with augmented neutrophil recruitment into affected joints and MMP activation.Conclusion. Circulating fibrocytes migrate to joints and influence the onset of disease processes in arthritis.

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Correlation of Plasma Interleukin 1 Levels With Disease Activity in Rheumatoid Arthritis

Cited by 450 publications

References 19 publications

RETRACTED: Cloricromene, a coumarine derivative, protects against collagen‐induced arthritis in Lewis rats

RETRACTED: Cloricromene, a coumarine derivative, protects against collagen‐induced arthritis in Lewis rats

Osteoprotegerin protects against generalized bone loss in tumor necrosis factor–transgenic mice

Circulating fibrocytes contribute to the pathogenesis of collagen antibody–induced arthritis

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