Erythema multiforme: a possible pathogenetic role of increased reactive oxygen species.
Recently, it has been suggested that reactive oxygen species (ROS) produced by activated polymorphonuclear leukocytes (PMNs) exert auto-oxidative tissue damage at the site of inflammation. In the present study, a possible role of ROS in the pathogenesis of erythema multiforme (EM) was investigated by determining the capacity of the sera from patients for generating ROS from PMNs. Significantly increased hydroxyl radical production was observed, which is one of the most potent ROS capable of causing tissue damage. This change was not observed when PMNs were incubated with sera from patients with bullous pemphigoid (BP) or inflammatory acne, indicating that this finding was not a common feature of immunologically mediated and/or inflammatory cutaneous disorders. Elevated C1q activities and depositions of immunoreactants in the blood vessels were also noticed in some patients. These findings suggest that ROS generated by PMNs are involved in the formation of cutaneous lesions of EM and that immune complexes (ICs) may provide an important mechanism in PMN activation.
D000328:Adult; D000368:Aged; D000936:Antigen-Antibody Complex / Q000032:analysis; D003166:Complement Activating Enzymes / Q000097:blood; D015922:Complement C1q; D003176:Complement C3 / Q000032:analysis; D004892:Erythema Multiforme / Q000097:blood* / Q000209:etiology / Q000276:immunology; D005260:Female; D005455:Fluorescent Antibody Technique; D006801:Humans; D007074:Immunoglobulin G / Q000032:analysis; D008297:Male; D008875:Middle Aged; D009504:Neutrophils / Q000145:classification / Q000276:immunology* / Q000378:metabolism; D010100:Oxygen / Q000378:metabolism*; D012867:Skin / Q000473:pathology
D000936:Antigen-Antibody Complex; D003176:Complement C3; D007074:Immunoglobulin G; D015922:Complement C1q; D003166:Complement Activating Enzymes; D010100:Oxygen