Messina Carlo G M, Reeves Emer P, Roes Jürgen, Segal Anthony W
Centre for Molecular Medicine, The Rayne Institute, University College London, 5 University Street, WC1E 6JJ, London, UK.
FEBS Lett. 2002 May 8;518(1-3):107-10. doi: 10.1016/s0014-5793(02)02658-3.
Myeloperoxidase-mediated chlorination is thought to be a necessary microbicidal mechanism. The H2O2 required for this process is generated by the NADPH oxidase. Staphylococcus aureus can also produce H2O2, which is not broken down by catalase negative organisms. It has been thought that this bacterial H2O2 can substitute for cellular H2O2 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 H2O2 they produced is insufficient to cause significant iodination, a marker for chlorination, thereby contradicting the accepted views on this subject.
髓过氧化物酶介导的氯化作用被认为是一种必要的杀菌机制。该过程所需的过氧化氢由NADPH氧化酶产生。金黄色葡萄球菌也能产生过氧化氢，而过氧化氢酶阴性的生物体不会将其分解。人们一直认为，在缺乏NADPH氧化酶的慢性肉芽肿病（CGD）中，这种细菌产生的过氧化氢可以在卤化反应中替代细胞过氧化氢。我们使用金黄色葡萄球菌过氧化氢酶阳性和阴性菌株的临床分离株，在CGD小鼠模型中重新探讨了这个问题。结果表明，这些生物体的毒力相当，它们产生的过氧化氢不足以引起显著的碘化反应（氯化作用的一个标志），从而与关于该主题的公认观点相矛盾。
