Chapter 16. Cellular Responses Mediating Chronic Inflammatory Diseases

Abstract

The etiology of chronic inflammatory diseases, such as rheumatoid arthritis, systemic lupus erythematosus, Crohn's disease, and sarcoidosis are discussed in this chapter. A chronic inflammatory component is recognized to occur in these diseases because of an influx of blood leukocytes and proliferation of the local cells. The synovial fluid of such joints is increased in volume and contains large numbers of polymorphonuclear leukocytes (PMN), lymphocytes, and macrophages. In addition to the cellular components present at the sites of inflammation, the products of various humoral systems associate with inflammatory events accumulate, fibrin, cleavage products of the complement system, kinins, and antigen–antibody complexes. Some inflammatory stimuli interact directly with phagocytic cells, causing the release of their mediators. Chronic inflammatory processes are the result of the interaction of a specific immunogenic stimulus with the lymphocytes. To develop meaningful assay systems to study the mechanisms involved in chronic inflammation, cells from cartilage, bone, normal synovium, and from organized inflammatory lesions as well as leukocytes from spleen, thymus, and macrophages from serous cavities of laboratory animals maintained as stable populations in cell or organ culture have been utilized. Recent improvements in the methodology for cell isolation from normal and inflamed tissues have permitted the maintenance of cell culture systems relevant to the situations. This is achieved by dispersing tissues by the judicious use of connective tissue degrading enzymes rather than mechanical disaggregation or mincing of tissue and incubation with trypsin.