Perpetuation of inflammation associated with experimental arthritis: the role of macrophage activation by neutrophilic myeloperoxidase. Issue 6 (1998)

• Record Type: Journal Article
• Authors: Gelderman, Monique P.; Stuart, Rodney; Vigerust, David; Fuhrmann, Steven; Lefkowitz, Doris L.; Allen, Robert C.; Lefkowitz, Stanley S.; Graham, Susan
• Is Part Of: Mediators of inflammation. Volume 7:Issue 6(1998)
• Page Start: 381
• Page End: 389
• Publication Date: 1998
• Subjects: Autoimmunity -- Peroxidases -- TNFα -- Rheumatoid arthritis -- Reactive oxygen intermediates; Inflammation -- Mediators -- Periodicals; Biological response modifiers -- Periodicals; Inflammation (Pathologie) -- Médiateurs; Immunomodulateurs; Biological response modifiers; Inflammation -- Mediators; Immunology; Autacoids; Immunologic Factors; Cell Adhesion Molecules; Cell Communication; Cytokines; Inflammation; Periodicals; Electronic journals; 616.0473
• DOI: 10.1080/09629359890758
• Languages: English
• ISSNs: 0962-9351

Abstract

Abstract : Rheumatoid arthritis (RA) is characterized by an abnormal cellular and cytokine infiltration of inflamed joints. This study addresses a previously unrecognized interaction between neutrophilic-myeloperoxidase (MPO) and macrophages (MΦ) which could explain the perpetuation of inflammation associated with RA. A monoarticular arthritis was induced in female Lewis rats by injection of streptococcal cell wall extracts (PG-APS). After swelling and erythema subsided, joints were re-injected with one of the following: porcine MPO or partially inactivated MPO (iMPO). Injection with either MPO or iMPO induced a 'flare' of experimental RA. Blocking the MΦ-mannose receptor by mannans, ablated exacerbation of disease. These results indicate that MPO or iMPO can play a pivotal role in the perpetuation but not initiation of this RA model.