Cell Tissue Damage Research Articles

Rheumatic aspects of acquired immunodeficiency syndrome.

Infection with HIV-1 continues to provide important insights into autoimmunity and rheumatic diseases. Studies on the mechanisms of B cell hyperreactivity in HIV-infected persons suggest a primary role for B cell complement receptor engagement by circulating immune complexes in the production of autoantibodies. Delineation of the epitopes recognized by antiphospholipid antibodies induced by HIV-1 offers insight into the mechanism of thrombosis associated with antiphospholipid antibodies found in the rheumatic diseases. Several reports have documented the coexistence of rheumatoid arthritis and HIV-1 infection, emphasizing the importance of both T cell-dependent and -independent mechanisms in the pathogenesis and clinical manifestations of rheumatoid arthritis. The mechanisms of host-virus interactions leading to rheumatic disease continue to be studied in HIV-infected persons with diffuse infiltrative lymphocytosis syndrome, a disease in which host immunogenetics appear to be the determining factor, and in persons with polymyositis. In both diseases, tissue cell damage appears to be a consequence of the host immune response to viral proteins present within macrophages in the target tissues. Because similar mechanisms appear to be involved in polymyositis associated with HTLV-I (human T cell lymphoma virus type I) infection, studies into a primate model of polymyositis induced by HTLV-I may be particularly informative. The clinical management of HIV-associated arthritides remains difficult, likely reflecting the role of HIV-1 gene products in initiating or amplifying inflammatory joint disease. Two anti-inflammatory drugs frequently used to treat patients with rheumatic diseases, indomethacin and hydroxychloroquine, can directly inhibit HIV-1 replication and may provide a rational therapeutic approach in combination with conventional antiviral agents.

Nimesulide as a downregulator of the activity of the neutrophil myeloperoxidase pathway. Focus on the histoprotective potential of the drug during inflammatory processes.

Neutrophils, recruited to tissue sites of inflammation, release a variety of oxidants and enzymes, which are responsible for tissue damage. Among the oxidants released are potent chlorinated compounds, such as hypochlorous acid and chloramines, which induce tissue cell damage and inactivate protease inhibitors, particularly alpha 1-antitrypsin, the specific inhibitor of neutrophil elastase. In studying a rational approach to the pharmacological control of neutrophil-mediated tissue injury, we investigated the activity of the anti-inflammatory drug nimesulide. This agent reduced the function of the myeloperoxidase pathway (which generates hypochlorous acid), by exerting a cell-directed inhibitory activity, as shown by measurement of superoxide anion and hydrogen peroxide production. Nimesulide also inactivated hypochlorous acid directly and protected alpha 1-antitrypsin from the neutrophil-mediated oxidation. Thus, neutrophil elastolytic activity may be attenuated by nimesulide-spared alpha 1-antitrypsin. The prevention of oxidative inactivation of alpha 1-antitrypsin by nimesulide strictly correlates with the drug's ability to suppress the extracellular availability of hypochlorous acid. Taken together, these data suggest that nimesulide may prevent tissue injury at sites of inflammation by maintaining natural host protective systems.

Effects of feeding experience on the odour‐conditioned anemotaxes of Colorado potato beetles

ences are significantly different it must be concluded that a strong aphid presence causes relatively little increase in the overall amount of cell damage. The length of time that aphids were allowed to feed hardly affected the amount of damage but it is possible that over substantially longer periods, such as experienced by a crop plant in the field, damage could accumulate. There was a noticable amount of cell damage in tissue not subjected to aphid attack. It seems most likely that this results from fixation of the plant material but the possibility exists that cells are influenced by other biological agencies such as leaf senescence or fungal infection. We conclude that in the short term aphid probing and feeding will not inflict substantial damage to the plant photosynthetic machinery and there is little suggestion that longer term problems will develop.