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活性氧(ROS)在人类抗分枝杆菌免疫效应机制中的作用。

The role of reactive oxygen species (ROS) in the effector mechanisms of human antimycobacterial immunity.

作者信息

Fazal N

机构信息

Department of Immunology, University of Birmingham, U.K.

出版信息

Biochem Mol Biol Int. 1997 Oct;43(2):399-408. doi: 10.1080/15216549700204191.

DOI:10.1080/15216549700204191
PMID:9350348
Abstract

The aim of this study was to determine the role of reactive oxygen species (ROS) in checking the growth of intracellular mycobacteria within human phagocytes. Peripheral blood-derived neutrophils and monocyte-derived macrophages were isolated from Chronic Granulomatous Disease (CGD) patients and normal healthy human volunteers. CGD patients are known to have a defect in the NADPH oxidase pathway, resulting in their neutrophils and monocyte-derived macrophages being unable to generate oxygen radicals which are required to kill intracellular bacteria. The cells were then infected with Bacille Calmette Guerin (BCG) or Mycobacterium avium, and the bacterial growth in each cell type determined by Colony Forming Units (CFU) estimate. The results obtained indicate that there was no demonstrable inhibition in the intracellular mycobacterial growth within neutrophils or macrophages derived from either Chronic Granulomatous Disease (CGD:deficient in NADPH oxidase pathway) or normal healthy volunteers. Macrophage treatment with either IFN-gamma or TNF-alpha had no effect.

摘要

本研究的目的是确定活性氧(ROS)在抑制人类吞噬细胞内细胞内分枝杆菌生长中的作用。从慢性肉芽肿病(CGD)患者和正常健康人类志愿者中分离出外周血来源的中性粒细胞和单核细胞来源的巨噬细胞。已知CGD患者的NADPH氧化酶途径存在缺陷,导致其嗜中性粒细胞和单核细胞衍生的巨噬细胞无法产生杀死细胞内细菌所需的氧自由基。然后用卡介苗(BCG)或鸟分枝杆菌感染细胞,并通过菌落形成单位(CFU)估计确定每种细胞类型中的细菌生长。获得的结果表明,源自慢性肉芽肿病(CGD:NADPH氧化酶途径缺陷)或正常健康志愿者的中性粒细胞或巨噬细胞内的细胞内分枝杆菌生长没有明显抑制。用IFN-γ或TNF-α处理巨噬细胞没有效果。

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