Jones G S, Amirault H J, Andersen B R
Department of Medicine, University of Illinois, Chicago.
J Infect Dis. 1990 Sep;162(3):700-4. doi: 10.1093/infdis/162.3.700.
To determine the role of oxygen radicals in the killing of Mycobacterium tuberculosis by neutrophils, the effects of free-radical inhibitors and enzymes, catalase, superoxide dismutase, taurine, deferoxamine, and histidine were evaluated. Changes in the viability of M. tuberculosis were determined by agar plate colony counts and a radiometric assay. No impairment in killing was seen with any of the inhibitors or enzymes. Patients with chronic granulomatous disease (CGD) have a defect in the NADPH oxidase pathway, causing their neutrophils to be unable to generate oxygen radicals. If these radicals are involved in killing, then CGD neutrophils should be less effective killers of M. tuberculosis than normal neutrophils. There was no evidence by either measure of M. tuberculosis viability that CGD neutrophils were less bactericidal than normal neutrophils. Killing by normal neutrophils was also effective in the absence of serum. These results lead to the conclusion that the mechanism by which M. tuberculosis is killed by neutrophils is independent of the oxygen metabolic burst.
为了确定氧自由基在中性粒细胞杀灭结核分枝杆菌中的作用，评估了自由基抑制剂和酶（过氧化氢酶、超氧化物歧化酶、牛磺酸、去铁胺和组氨酸）的作用。通过琼脂平板菌落计数和放射性测定法确定结核分枝杆菌活力的变化。未观察到任何抑制剂或酶对杀灭作用有损害。慢性肉芽肿病（CGD）患者的NADPH氧化酶途径存在缺陷，导致其中性粒细胞无法产生氧自由基。如果这些自由基参与杀灭过程，那么CGD中性粒细胞作为结核分枝杆菌的杀手应比正常中性粒细胞效率更低。通过任何一种结核分枝杆菌活力测定方法均未发现证据表明CGD中性粒细胞的杀菌能力低于正常中性粒细胞。在无血清的情况下，正常中性粒细胞的杀灭作用也有效。这些结果得出结论，中性粒细胞杀灭结核分枝杆菌的机制与氧代谢爆发无关。
