Chemotactic factor inactivation by stimulated human neutrophils mediated by myeloperoxidase-catalyzed methionine oxidation.

摘要: Leukocyte chemoattractants were inactivated when exposed to human neutrophils and either ingestible particles or phorbol esters. Loss of biologic activity was time- temperature-dependent, required physiologic concentrations viable a halide, inhibited by azide catalase. Neutrophils from patients with hereditary myeloperoxidase deficiency chronic granulomatous disease failed inactivate the unless purified H2O2, respectively, added. Susceptibility inactivation correlated presence methionine in attractant. chemotactic blocked low higher other reducing agents, but unaffected oxidized methionine. Paper chromatography demonstrated that exposure formyl-methionyl peptide factor cellfree system stimulated resulted its conversion molecular species whose location chromatographs identical containing Thus, secretion which combine halides form oxidants react critical residue. We suggest myeloperoxidase-catalyzed oxidation thioethers may constitute an inflammatory control mechanism as well general means modifying functional properties mediators.