Authors: David Alan Thompson Bruce D Hammock
Publish Date: 2007/03/01
Volume: 32, Issue: 2, Pages: 279-291
Abstract
The leukotoxins 910and 1213EpOME are produced by activated inflammatory leukocytes such as neutrophils High EpOME levels are observed in disorders such as acute respiratory distress syndrome and in patients with extensive burns Although the physiological significance of the EpOMEs remains poorly understood in some systems the EpOMEs act as a protoxin with their corresponding epoxide hydrolase metabolites 910and 1213DiHOME specifically exerting toxicity Both the EpOMEs and the DiHOMEs were also recently shown to have neutrophil chemotactic activity We evaluated whether the neutrophil respiratory burst a surge of oxidant production thought to play an important role in limiting certain bacterial and fungal infections is modulated by members of the EpOME metabolic pathway We present evidence that the DiHOMEs suppress the neutrophil respiratory burst by a mechanism distinct from that of respiratory burst inhibitors such as cyclosporin H or lipoxin A4 which inhibit multiple aspects of neutrophil activation
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