Characterization of pristane‐induced arthritis, a murine model of chronic disease: Response to antirheumatic agents, expression of joint cytokines, and immunopathology

Patten, Christopher; Bush, K. A.; Rioja, Inma; Morgan, Rebecca; Wooley, Paul H.; Trill, John J.; Life, Paul

doi:10.1002/art.20507

Cited by 66 publications

(57 citation statements)

References 31 publications

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“…Our studies and the literature (35) indicate that this dosing effectively blocks TNF-a in mice without apparent toxicities. A much lower dose (10 Ag/animal f0.4 mg/kg), comparable with the one used in humans, was also effective in reducing intrapleural tumor dissemination and pleural fluid accumulation in the mouse model of LLC-induced MPE.…”

Section: Discussionsupporting

confidence: 66%

“…For in vivo TNF-a neutralization, mice received i.p. 300 Ag sTNFR:Fc/100 AL vehicle (control, 100 AL vehicle) on days 3, 5, 7, 9, 11, and 13 after LLC cells, a dosing reported to effectively neutralize TNF-a (35). In a separate dose-response experiment, mice received 0, 10, 100, or 300 Ag sTNFR:Fc/100 AL vehicle on days 3, 5, 7, 9, 11, and 13 after LLC cells.…”

Section: Methodsmentioning

confidence: 99%

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Tumor Necrosis Factor-α Promotes Malignant Pleural Effusion

Stathopoulos

Kollintza²,

Moschos³

et al. 2007

Cancer Research

100

121

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Tumor necrosis factor (TNF)-A is present in the microenvironment of human tumors, including malignant pleural effusion (MPE). Although the cytokine is produced in the pleural cavity by both tumor and host cells, its effects on MPE formation are unknown. In these studies, we sought to determine the role of TNF-A in the pathogenesis of MPE and to assess the therapeutic effects of its neutralization in a preclinical model. For this, MPEs were generated in immunocompetent mice using intrapleural injection of mouse lung adenocarcinoma cells. The roles of tumor-and host-derived TNF-A were assessed using combined experimentation with TNF-a gene-deficient mice and in vivo TNF-A neutralization.

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Section: Discussionsupporting

confidence: 66%

Section: Methodsmentioning

confidence: 99%

Tumor Necrosis Factor-α Promotes Malignant Pleural Effusion

Stathopoulos

Kollintza²,

Moschos³

et al. 2007

Cancer Research

100

121

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“…These observations have stimulated research on inhibitors of p38 MAPK as potential antiinflammatory drug therapy. Indeed, p38 MAPK inhibitors have been successfully tested in animal models of arthritis, such as collagen-induced arthritis, and have also passed early-phase clinical trials (23,24). Many of these studies have supported the concept that p38 MAPK is importantly involved in the production of proinflammatory cytokines upon initiation of inflammatory arthritis.…”

Section: Discussionmentioning

confidence: 99%

Activation of p38 MAPK is a key step in tumor necrosis factor–mediated inflammatory bone destruction

Zwerina¹,

Hayer²,

Redlich³

et al. 2006

Arthritis & Rheumatism

133

107

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Objective. To investigate whether activation of p38 MAPK is a crucial signaling factor in inflammatory bone destruction mediated by tumor necrosis factor (TNF). Mice overexpressing TNF were treated with 2 different inhibitors of p38 MAPK, and the effect of this treatment on joint inflammation and structural damage was assessed.Methods. Human TNF-transgenic mice received systemic treatment with 2 different p38 MAPK inhibitors (RO4399247 and AVE8677). Treatment was started at the time of symptom onset and lasted for 6 weeks. Mice were assessed for clinical signs of arthritis, bone erosion, and cartilage damage. In addition, the effect of these inhibitors on osteoclast generation in vitro and in vivo was assessed.Results. Both p38 MAPK inhibitors significantly reduced clinical signs of TNF-mediated arthritis. This was attributable to reducing synovial inflammation by 50% without affecting the cellular composition of the infiltrate. Synovial expression of interleukin-1 and RANKL was reduced upon p38 MAPK blockade, and activation of the molecular target MAPK-activated protein kinase 2 (MAPKAP-2) was also inhibited. Proteoglycan loss of articular cartilage was reduced by 50%, although p38 MAPK inhibition did not change matrix molecule synthesis by cultivated chondrocytes. Importantly, bone loss was almost completely prevented by p38 MAPK inhibition. The numbers of synovial osteoclasts and precursors were dramatically reduced, and both p38 MAPK inhibitors also inhibited in vitro osteoclastogenesis at micromolar concentrations and blocked activation of MAPKAP-2 as well as differentiation markers in cultured osteoclast precursors.Conclusion. These results suggest the major importance of p38 MAPK for TNF-mediated inflammatory bone destruction in arthritis and suggest that inhibition of p38 MAPK might be an important tool for reducing structural damage in rheumatoid arthritis.

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“…Because the response to TNF-a targeted therapy is limited in pristane-induced arthritis, this model is valuable for the study of therapies relevant to patients who do not respond to TNF-a inhibitors. 43 …”

Section: Polyarthritis In the Context Of Chronic Inflammationmentioning

confidence: 99%

Mouse Models of Rheumatoid Arthritis

Caplazi¹,

Baca²,

Barck³

et al. 2015

Vet Pathol

117

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Rheumatoid arthritis (RA) is a chronic debilitating autoimmune disorder characterized by synovitis that leads to cartilage and bone erosion by invading fibrovascular tissue. Mouse models of RA recapitulate many features of the human disease. Despite the availability of medicines that are highly effective in many patient populations, autoimmune diseases (including RA) remain an area of active biomedical research, and consequently mouse models of RA are still extensively used for mechanistic studies and validation of therapeutic targets. This review aims to integrate morphologic features with model biology and cover the key characteristics of the most commonly used induced and spontaneous mouse models of RA. Induced models emphasized in this review include collagen-induced arthritis and antibody-induced arthritis. Collagen-induced arthritis is an example of an active immunization strategy, whereas antibody-induced arthritis models, such as collagen antibody-induced arthritis and K/BxN antibody transfer arthritis, represent examples of passive immunization strategies. The coverage of spontaneous models in this review is focused on the TNFD ARE mouse, in which arthritis results from overexpression of TNF-a, a master proinflammatory cytokine that drives disease in many patients.

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Characterization of pristane‐induced arthritis, a murine model of chronic disease: Response to antirheumatic agents, expression of joint cytokines, and immunopathology

Cited by 66 publications

References 31 publications

Tumor Necrosis Factor-α Promotes Malignant Pleural Effusion

Tumor Necrosis Factor-α Promotes Malignant Pleural Effusion

Activation of p38 MAPK is a key step in tumor necrosis factor–mediated inflammatory bone destruction

Mouse Models of Rheumatoid Arthritis

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