Auto-oxidative damage in Behçet's disease--endothelial cell damage following the elevated oxygen radicals generated by stimulated neutrophils.
The functions of phagocytes are enhanced in patients with Behçet's disease, therefore, we investigated the neutrophil-derived oxygen intermediates (OI) and lysosomal enzymes from 17 patients receiving glucocorticosteroids (steroids) and colchicine. Cultured endothelial cells were incubated with neutrophils to assess tissue injury. In cases of the complete type, in the active stage of the disease, OI production was markedly increased. The other patients showed significantly higher OI and higher lysosomal enzyme levels than patients with other diseases (controls) receiving drug therapy. Cytotoxicity tests showed that the 51Cr release was also significantly higher. The destruction of desmosomes and cell deformation were demonstrated electron microscopically. The simultaneous addition of superoxide dismutase and catalase in the cell culture decreased the 51Cr release to control levels. These findings suggest that neutrophils from patients with Behçet's disease generate high levels of OI, resulting in endothelial tissue damage.
D000293:Adolescent; D000328:Adult; D001528:Behcet Syndrome / Q000097:blood* / Q000276:immunology / Q000473:pathology; D003602:Cytotoxicity, Immunologic; D004727:Endothelium / Q000648:ultrastructure; D005260:Female; D005966:Glucuronidase / Q000096:biosynthesis; D006801:Humans; D006861:Hydrogen Peroxide / Q000097:blood; D008163:Luminescent Measurements; D008297:Male; D008854:Microscopy, Electron; D008875:Middle Aged; D009113:Muramidase / Q000096:biosynthesis; D009504:Neutrophils / Q000276:immunology / Q000378:metabolism*; D010101:Oxygen Consumption
D006861:Hydrogen Peroxide; D009113:Muramidase; D005966:Glucuronidase