KILLING OF MYCOBACTERIUM-TUBERCULOSIS BY NEUTROPHILS - A NONOXIDATIVE PROCESS
KILLING OF MYCOBACTERIUM-TUBERCULOSIS BY NEUTROPHILS - A NONOXIDATIVE PROCESS
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DOI：
10.1093/infdis/162.3.700
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发表时间：
1990-09-01
影响因子：
6.4
通讯作者：
ANDERSEN, BR
中科院分区：
文献类型：
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作者：
JONES, GS;AMIRAULT, HJ;ANDERSEN, BR
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，对自由基抑制剂和酶、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进行了评价。用琼脂平板菌落培养法和放射测定法测定结核分枝杆菌存活率的变化。没有发现任何抑制剂或酶对杀戮造成损害。慢性肉芽肿性疾病(CGD)患者的NADPH氧化酶途径存在缺陷，导致他们的中性粒细胞无法产生氧自由基。如果这些自由基参与了杀戮，那么CGD中性粒细胞应该比正常的中性粒细胞更不能有效地杀死结核分枝杆菌。两种衡量结核分枝杆菌活性的方法都没有证据表明CGD中性粒细胞比正常中性粒细胞杀菌能力低。在没有血清的情况下，正常中性粒细胞的杀伤也是有效的。这些结果得出的结论是，中性粒细胞杀死结核分枝杆菌的机制与氧代谢爆发无关。
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 courts 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.