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Adjuvant Arthritis

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Eric F Morand – One of the best experts on this subject based on the ideXlab platform.

  • involvement of macrophage migration inhibitory factor in the evolution of rat Adjuvant Arthritis
    Arthritis & Rheumatism, 1998
    Co-Authors: Michelle Theresa Leech, Christine N. Metz, Leilani Llanes Santos, Tina Peng, Stephen R. Holdsworth, Richard Bucala, Eric F Morand
    Abstract:

    Objective Recent studies have established an essential role for macrophage migration inhibitory factor (MIF) in T cell and macrophage activation, both of which are characteristics of rat Adjuvant Arthritis. This study investigated the role of MIF in early Adjuvant Arthritis. Methods MIF was detected in rat synovium by immunohistochemistry and enzyme-linked immunosorbent assay using specific monoclonal antibodies (MAb). Anti-MIF MAb treatment was administered, and the effects on clinical aspects of Adjuvant Arthritis were assessed. Results MIF was absent from normal rat synovium prior to Adjuvant injection, but was detectable on day 4 after injection (6 days before the onset of clinical disease) and was colocalized with ED-1 + macrophages throughout the evolution of the disease. Levels of MIF were increased in established Adjuvant Arthritis sera, and Adjuvant Arthritis synovial macrophages released MIF at a mean ± SEM concentration of 607.9 ± 201.5 pg/ml. Anti-MIF treatment led to profound, dose-dependent inhibition of the Adjuvant Arthritis clinical score, paw swelling, and synovial lavage leukocyte numbers (P < 0.001), and also resulted in reduced synovial macrophage and T cell accumulation. Conclusion These findings demonstrate an important role for MIF in the evolution of rat Adjuvant Arthritis.

  • Involvement of macrophage migration inhibitory factor in the evolution of rat Adjuvant Arthritis.
    Arthritis and rheumatism, 1998
    Co-Authors: Michelle Theresa Leech, Christine N. Metz, Leilani Llanes Santos, Tina Peng, Stephen R. Holdsworth, Richard Bucala, Eric F Morand
    Abstract:

    Recent studies have established an essential role for macrophage migration inhibitory factor (MIF) in T cell and macrophage activation, both of which are characteristics of rat Adjuvant Arthritis. This study investigated the role of MIF in early Adjuvant Arthritis. MIF was detected in rat synovium by immunohistochemistry and enzyme-linked immunosorbent assay using specific monoclonal antibodies (MAb). Anti-MIF MAb treatment was administered, and the effects on clinical aspects of Adjuvant Arthritis were assessed. MIF was absent from normal rat synovium prior to Adjuvant injection, but was detectable on day 4 after injection (6 days before the onset of clinical disease) and was colocalized with ED-1+ macrophages throughout the evolution of the disease. Levels of MIF were increased in established Adjuvant Arthritis sera, and Adjuvant Arthritis synovial macrophages released MIF at a mean +/- SEM concentration of 607.9 +/- 201.5 pg/ml. Anti-MIF treatment led to profound, dose-dependent inhibition of the Adjuvant Arthritis clinical score, paw swelling, and synovial lavage leukocyte numbers (P < 0.001), and also resulted in reduced synovial macrophage and T cell accumulation. These findings demonstrate an important role for MIF in the evolution of rat Adjuvant Arthritis.

Michelle Theresa Leech – One of the best experts on this subject based on the ideXlab platform.

  • involvement of macrophage migration inhibitory factor in the evolution of rat Adjuvant Arthritis
    Arthritis & Rheumatism, 1998
    Co-Authors: Michelle Theresa Leech, Christine N. Metz, Leilani Llanes Santos, Tina Peng, Stephen R. Holdsworth, Richard Bucala, Eric F Morand
    Abstract:

    Objective Recent studies have established an essential role for macrophage migration inhibitory factor (MIF) in T cell and macrophage activation, both of which are characteristics of rat Adjuvant Arthritis. This study investigated the role of MIF in early Adjuvant Arthritis. Methods MIF was detected in rat synovium by immunohistochemistry and enzyme-linked immunosorbent assay using specific monoclonal antibodies (MAb). Anti-MIF MAb treatment was administered, and the effects on clinical aspects of Adjuvant Arthritis were assessed. Results MIF was absent from normal rat synovium prior to Adjuvant injection, but was detectable on day 4 after injection (6 days before the onset of clinical disease) and was colocalized with ED-1 + macrophages throughout the evolution of the disease. Levels of MIF were increased in established Adjuvant Arthritis sera, and Adjuvant Arthritis synovial macrophages released MIF at a mean ± SEM concentration of 607.9 ± 201.5 pg/ml. Anti-MIF treatment led to profound, dose-dependent inhibition of the Adjuvant Arthritis clinical score, paw swelling, and synovial lavage leukocyte numbers (P < 0.001), and also resulted in reduced synovial macrophage and T cell accumulation. Conclusion These findings demonstrate an important role for MIF in the evolution of rat Adjuvant Arthritis.

  • Involvement of macrophage migration inhibitory factor in the evolution of rat Adjuvant Arthritis.
    Arthritis and rheumatism, 1998
    Co-Authors: Michelle Theresa Leech, Christine N. Metz, Leilani Llanes Santos, Tina Peng, Stephen R. Holdsworth, Richard Bucala, Eric F Morand
    Abstract:

    Recent studies have established an essential role for macrophage migration inhibitory factor (MIF) in T cell and macrophage activation, both of which are characteristics of rat Adjuvant Arthritis. This study investigated the role of MIF in early Adjuvant Arthritis. MIF was detected in rat synovium by immunohistochemistry and enzyme-linked immunosorbent assay using specific monoclonal antibodies (MAb). Anti-MIF MAb treatment was administered, and the effects on clinical aspects of Adjuvant Arthritis were assessed. MIF was absent from normal rat synovium prior to Adjuvant injection, but was detectable on day 4 after injection (6 days before the onset of clinical disease) and was colocalized with ED-1+ macrophages throughout the evolution of the disease. Levels of MIF were increased in established Adjuvant Arthritis sera, and Adjuvant Arthritis synovial macrophages released MIF at a mean +/- SEM concentration of 607.9 +/- 201.5 pg/ml. Anti-MIF treatment led to profound, dose-dependent inhibition of the Adjuvant Arthritis clinical score, paw swelling, and synovial lavage leukocyte numbers (P < 0.001), and also resulted in reduced synovial macrophage and T cell accumulation. These findings demonstrate an important role for MIF in the evolution of rat Adjuvant Arthritis.

J. Urban Lindgren – One of the best experts on this subject based on the ideXlab platform.

  • Galanin in Adjuvant Arthritis in the rat.
    The Journal of rheumatology, 2004
    Co-Authors: Wu Qinyang, Kjell Hultenby, Elhassan Adlan, J. Urban Lindgren
    Abstract:

    To study the concentration changes of galanin in the ankles and spinal cord and to detect the distribution of galanin in different tissues in arthritic rats. Adjuvant Arthritis was induced by intradermal injection of Mycobacterium butyricum in Freund’s incomplete Adjuvant at the base of the tail. The concentrations of galanin were measured by radioimmunoassay (RIA) and the distributions of galanin were detected by immunoelectron microscopy (iEM). Measurements were taken on Day 28 after injection. RIA results showed that the concentration of galanin was significantly lower in the ankles and spinal cords of rats with Adjuvant Arthritis compared to controls. Our iEM results showed a heterogeneous distribution of galanin labelling in different cells and tissue compartments. In arthritic rats, we observed decreased galanin labelling in the sciatic nerve and in macrophage-like cells in the synovial membrane and increased labelling in monocyte lineage cells, polymorphonucleated lineage cells in the bone marrow, fibroblasts in the periosteum, osteoclasts and osteocytes, and lower labelling in osteoblasts compared to controls. Galanin is involved in the response to inflammation in Adjuvant Arthritis and might play a role in the regulation of inflammation and nociception. These findings are in accordance with a biological role of galanin in the development of inflammatory Arthritis.

  • Intracerebroventricular administration of somatostatin prevents and attenuates Adjuvant Arthritis.
    Journal of neuroimmunology, 2001
    Co-Authors: Adlan M. Elhassan, Abdu Adem, Nikos Papadogiannakis, Suliman Isam A, Adel Gad, J. Urban Lindgren
    Abstract:

    The effects of somatostatin on the development of Adjuvant Arthritis induced by Mycobacterium butyricum were studied. Somatostatin was injected into the lateral cerebral ventricle every day for 14 days beginning on the first day of mycobacteria inoculation in the preventive group. In the treatment group, somatostatin was injected from day 17 until day 30 post-mycobacteria inoculation. Arthritis was evaluated by measuring ankle joint circumference and diameter as well as microscopic examination of ankle joint sections. Somatostatin profoundly inhibited the development of Adjuvant Arthritis and an anti-inflammatory action was observed in the treatment group. These results suggest that somatostatin has a central action that can prevent or attenuate symptoms associated with Arthritis.

  • Intracerebroventricular met-enkephalin administration modulates Adjuvant Arthritis.
    Brain Research, 2000
    Co-Authors: Adlan M. Elhassan, Abdu Adem, Nikos Papadogiannakis, Suliman Isam A, Adel Gad, J. Urban Lindgren
    Abstract:

    The purpose of this study was to investigate the anti-inflammatory properties of intracerebroventricular met-enkephalin (met-enk) administration in an animal model of Arthritis. Adjuvant Arthritis was induced in rats by intradermal inoculation of mycobacterium butyricum and the effects of intraventricular met-enk+thiorphan (enkephalinase inhibitor) were studied. Treatment was initiated either simultaneously with the bacterial inoculation (preventive group) or on post-inoculation day 17 after the appearance of inflammation (treatment group). The degree of inflammation was evaluated by measuring the diameter and the circumference of the ankle joint immediately before the sacrifice (day 31) and by histologic examination of ankle joint sections. The results of this study revealed that combined intraventricular injections of met-enk+thiorphan reduced the arthritic-like inflammation in the preventive group as well as in the treatment group. These findings suggest that centrally applied met-enk+thiorphan may suppress the development Adjuvant Arthritis as well as the symptoms of manifest Arthritis. Thus central met-enk may be involved in both hypothalamic pituitary adrenal axis and immune forms of stress-induced modulation.

Toshio Fukuda – One of the best experts on this subject based on the ideXlab platform.

  • Effects of FR167653, a dual inhibitor of interleukin-1 and tumor necrosis factor, on Adjuvant Arthritis in rats.
    Modern rheumatology, 2001
    Co-Authors: Tetsuya Shinozaki, Kenji Takagishi, Satoshi Tsutsumi, Takashi Yanagawa, Kimihiko Takeuchi, Hideomi Watanabe, Toshio Fukuda
    Abstract:

    The effects of FR167653, a dual inhibitor of interleukin (IL)-1β and tumor necrnecrosistor (TNF)-α production, on the development of Adjuvant Arthritis were investigated in rats. Female Sprague–Dawleys rats weighing 130 g with Adjuvant Arthritis were administered FR167653 0.1, 1, 10, or 30 mg/kg, and their Arthritis scores, soft tissue X-rays, and histological findings were then compared with those of a control group. Body weights were also recorded. FR167653 suppressed the severity of Adjuvant Arthritis in a dose-dependent manner. Administration of the drug had little effect on body weight. FR167653 might locally affect arthritic joints to prevent inflammation. However, further experiments are necessary to elucidate the underlying mechanisms.

Stephen R. Holdsworth – One of the best experts on this subject based on the ideXlab platform.

  • involvement of macrophage migration inhibitory factor in the evolution of rat Adjuvant Arthritis
    Arthritis & Rheumatism, 1998
    Co-Authors: Michelle Theresa Leech, Christine N. Metz, Leilani Llanes Santos, Tina Peng, Stephen R. Holdsworth, Richard Bucala, Eric F Morand
    Abstract:

    Objective Recent studies have established an essential role for macrophage migration inhibitory factor (MIF) in T cell and macrophage activation, both of which are characteristics of rat Adjuvant Arthritis. This study investigated the role of MIF in early Adjuvant Arthritis. Methods MIF was detected in rat synovium by immunohistochemistry and enzyme-linked immunosorbent assay using specific monoclonal antibodies (MAb). Anti-MIF MAb treatment was administered, and the effects on clinical aspects of Adjuvant Arthritis were assessed. Results MIF was absent from normal rat synovium prior to Adjuvant injection, but was detectable on day 4 after injection (6 days before the onset of clinical disease) and was colocalized with ED-1 + macrophages throughout the evolution of the disease. Levels of MIF were increased in established Adjuvant Arthritis sera, and Adjuvant Arthritis synovial macrophages released MIF at a mean ± SEM concentration of 607.9 ± 201.5 pg/ml. Anti-MIF treatment led to profound, dose-dependent inhibition of the Adjuvant Arthritis clinical score, paw swelling, and synovial lavage leukocyte numbers (P < 0.001), and also resulted in reduced synovial macrophage and T cell accumulation. Conclusion These findings demonstrate an important role for MIF in the evolution of rat Adjuvant Arthritis.

  • Involvement of macrophage migration inhibitory factor in the evolution of rat Adjuvant Arthritis.
    Arthritis and rheumatism, 1998
    Co-Authors: Michelle Theresa Leech, Christine N. Metz, Leilani Llanes Santos, Tina Peng, Stephen R. Holdsworth, Richard Bucala, Eric F Morand
    Abstract:

    Recent studies have established an essential role for macrophage migration inhibitory factor (MIF) in T cell and macrophage activation, both of which are characteristics of rat Adjuvant Arthritis. This study investigated the role of MIF in early Adjuvant Arthritis. MIF was detected in rat synovium by immunohistochemistry and enzyme-linked immunosorbent assay using specific monoclonal antibodies (MAb). Anti-MIF MAb treatment was administered, and the effects on clinical aspects of Adjuvant Arthritis were assessed. MIF was absent from normal rat synovium prior to Adjuvant injection, but was detectable on day 4 after injection (6 days before the onset of clinical disease) and was colocalized with ED-1+ macrophages throughout the evolution of the disease. Levels of MIF were increased in established Adjuvant Arthritis sera, and Adjuvant Arthritis synovial macrophages released MIF at a mean +/- SEM concentration of 607.9 +/- 201.5 pg/ml. Anti-MIF treatment led to profound, dose-dependent inhibition of the Adjuvant Arthritis clinical score, paw swelling, and synovial lavage leukocyte numbers (P < 0.001), and also resulted in reduced synovial macrophage and T cell accumulation. These findings demonstrate an important role for MIF in the evolution of rat Adjuvant Arthritis.