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Reactive metabolites of oxygen and nitrogen, adhesion molecule expression and chronic joint inflammation

  • Chapter
Free Radicals and Inflammation

Part of the book series: Progress in Inflammation Research ((PIR))

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Abstract

One of the hallmark features of rheumatoid arthritis (RA) is the infiltration of large numbers of mononuclear leukocytes (monocytes, lymphocytes) into the inflamed synovium. In addition, extensive polymorphonuclear leukocyte (neutrophil) infiltration is observed in synovial fluid. This inflammatory infiltrate is accompanied by extensive articular damage including cartilage and bone erosion, edema and enhanced vascular permeability suggesting an important role for these leukocytes in the pathophysiology of RA. Recent studies have demonstrated that the enhanced leukocyte infiltrate and some of the pathophysiology observed in different models of synovitis and in human RA may be mediated by the interaction between leukocytes and specific endothelial cell adhesion molecules (ECAMs) [1-6]. These observations have prompted us to propose that the synovial microvasculature regulates chronic joint inflammation by virtue of its ability to modulate the infiltration of immune-modulating and/or potentially injurious leukocytes into the synovial interstitium. Indeed, one of the earliest histopathological events observed in the development of RA is activation and/or injury to the endothelial cell lining of the synovial microvasculature [7 9].This discussion will review the data implicating ECAMs as important determinants in the pathogenesis of RA and discuss the molecular mechanisms that regulate ECAM expression in the chronically inflamed joint, and indicate the roles of oxygen-and nitrogen-derived free radicals in these processes.

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Authors and Affiliations

  1. Departments of Molecular and Cellular Physiology, 1501 Kings Highway, P.O. Box 33932, Shreveport, LA 71130-3932, USA

    Matthew B. Grisham

  2. Departments of Medicine, Louisiana State University Medical Center, 1501 Kings Highway, P.O. Box 33932, Shreveport, LA 71130-3932, USA

    Robert E. Wolf

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  1. St. Bartholomew’s and The Royal London School of Medicine and Dentistry, Queen Mary and Westfield College, 25-29 Ashfield Street, London, E1 1AD, UK

    Paul G. Winyard

  2. School of Postgraduate Medicine, University of Bath, Claverton Down, Bath, BA2 7AY, UK

    David R. Blake

  3. Musculoskeletal Institute, University of Pittsburgh School of Medicine, 986 Scaife Hall, Pittsburgh, 15261, PA, USA

    Christopher H. Evans

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Grisham, M.B., Wolf, R.E. (2000). Reactive metabolites of oxygen and nitrogen, adhesion molecule expression and chronic joint inflammation. In: Winyard, P.G., Blake, D.R., Evans, C.H. (eds) Free Radicals and Inflammation. Progress in Inflammation Research. Birkhäuser, Basel. https://doi.org/10.1007/978-3-0348-8482-2_8

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  • DOI: https://doi.org/10.1007/978-3-0348-8482-2_8

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