Neutrophil-generated active oxygens in linear IgA bullous dermatosis.
To examine the possible correlation between tissue injury and neutrophil-produced active oxygens (AOs) in patients with linear IgA bullous dermatosis (BD), we studied the capacity of neutrophils from six patients with BD to generate AOs. Cultured endothelial cells from human umbilical-cord vein were also incubated with the patients' neutrophils to assess AO-induced tissue injury. The AO production by patients' neutrophils was significantly elevated. The patients' neutrophils, as well as those from healthy controls preincubated with patients' serum, produced significantly increased levels of cytotoxic response on coincubation with chromium 51-labeled human endothelial cells. These results suggest that the tissue damage observed in BD may be partially due to both excessive production of AOs by neutrophils and a serum factor present in the patients, and further postulate the similar pathogenic process in dermatitis herpetiformis.
D000293:Adolescent; D000328:Adult; D003601:Cytotoxicity Tests, Immunologic; D005260:Female; D005966:Glucuronidase / Q000378:metabolism; D006801:Humans; D006861:Hydrogen Peroxide / Q000378:metabolism; D007070:Immunoglobulin A; D009113:Muramidase / Q000378:metabolism; D009504:Neutrophils / Q000201:enzymology / Q000378:metabolism* / Q000502:physiology; D010100:Oxygen / Q000378:metabolism*; D012872:Skin Diseases, Vesiculobullous / Q000276:immunology*; D015054:Zymosan / Q000494:pharmacology
D007070:Immunoglobulin A; D015054:Zymosan; D006861:Hydrogen Peroxide; D009113:Muramidase; D005966:Glucuronidase; D010100:Oxygen