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人类免疫缺陷病毒感染中中性粒细胞超氧化物生成受抑制

Depressed neutrophil superoxide production in human immunodeficiency virus infection.

作者信息

Pitrak D L, Bak P M, DeMarais P, Novak R M, Andersen B R

机构信息

Department of Medicine, University of Illinois College of Medicine, Chicago.

出版信息

J Infect Dis. 1993 Jun;167(6):1406-10. doi: 10.1093/infdis/167.6.1406.

Abstract

Neutrophil (PMNL) superoxide (O2-) production was evaluated in 71 patients with human immunodeficiency virus (HIV) infection at different stages of disease. In vitro O2- production was significantly depressed for PMNL isolated from HIV-positive patients compared with control PMNL at rest and after stimulation. The degree of impairment of O2- production was more pronounced for patients with lower absolute CD4+ lymphocyte counts. Antiretroviral therapy with zidovudine was also associated with impaired O2- production, but this may reflect a longer duration of disease for treated patients. Zidovudine had no direct inhibitory effect on O2- production by control PMNL in vitro, and serial measurements of O2- production by PMNL from patients before and after initiation of zidovudine did not demonstrate an in vivo inhibitory effect. Impaired PMNL oxidative metabolism in HIV infection may contribute to the increased risk of serious bacterial infections, certain opportunistic infections, and perhaps the pathogenesis of HIV infection itself.

摘要

在71例处于疾病不同阶段的人类免疫缺陷病毒(HIV)感染患者中,评估了中性粒细胞(PMNL)超氧化物(O2-)的产生情况。与静息状态及刺激后的对照PMNL相比,从HIV阳性患者分离出的PMNL的体外O2-产生显著降低。对于绝对CD4+淋巴细胞计数较低的患者,O2-产生的受损程度更为明显。齐多夫定抗逆转录病毒疗法也与O2-产生受损有关,但这可能反映了接受治疗患者的病程较长。齐多夫定在体外对对照PMNL的O2-产生没有直接抑制作用,并且在齐多夫定治疗前后对患者PMNL的O2-产生进行的系列测量未显示出体内抑制作用。HIV感染中PMNL氧化代谢受损可能导致严重细菌感染、某些机会性感染风险增加,或许还与HIV感染本身的发病机制有关。

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