Abstract
Myeloperoxidase-mediated chlorination is thought to be a necessary microbicidal mechanism. The H 2O 2 required for this process is generated by the NADPH oxidase. Staphylococcus aureus can also produce H 2O 2, which is not broken down by catalase negative organisms. It has been thought that this bacterial H 2O 2 can substitute for cellular H 2O 2 in the halogenation reaction in chronic granulomatous disease (CGD) where neutrophils are lacking the NADPH oxidase. We have readdressed this issue in a mouse model of CGD using clinical isolates of catalase positive and negative strains of S. aureus. The results showed these organisms to be equally virulent and that the H 2O 2 they produced is insufficient to cause significant iodination, a marker for chlorination, thereby contradicting the accepted views on this subject.
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