Early induction and late abrogation of respiratory burst in A-phagocytophilum -: Infected neutrophils
Early induction and late abrogation of respiratory burst in A-phagocytophilum -: Infected neutrophils
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DOI：
10.1111/j.1749-6632.2003.tb07415.x
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发表时间：
2003-01-01
期刊：
影响因子：
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通讯作者：
Dumler, JS
中科院分区：
文献类型：
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作者：
Choi, KS;Dumler, JS
人粒细胞埃立克体病是一种由嗜吞噬细胞无形体引起的蜱传疾病。这种微生物是独特的，因为它在中性粒细胞空泡中存活和繁殖。在吞噬过程中，专职吞噬细胞通过NADPH氧化酶的活性增加耗氧量（呼吸爆发），NADPH氧化酶产生超氧阴离子（O-2（-））和过氧化氢（H2 O2）。我们测定了A.通过使用2 '，7'-二氯二氢荧光素二乙酸酯（DCFH-DA），一种通常用于检测活性氧（ROS）的细胞产生的荧光探针，检测嗜吞噬细胞感染的中性粒细胞响应早期感染（0、3和5小时）产生O-2（-）。我们的流式细胞仪分析表明，无细胞A。嗜吞噬细胞菌诱导的呼吸爆发是LPS的6.9倍，3小时后仍有较低程度的明显作用，但5小时后消失。A.嗜吞噬细胞菌首先诱导然后抑制中性粒细胞的呼吸爆发。呼吸爆发活动的长期减少可能对A.嗜吞噬细胞菌和中性粒细胞中的其他感染因子。其作用可能是产生一种功能有限的慢性肉芽肿性疾病，易受机会性病原体感染。
Human granulocytic ehrlichiosis is an emerging tick-borne disease caused by the obligate intracellular pathogen, Anaplasma phagocytophilum. This organism is unique because it survives and propagates in neutrophil vacuoles. During phagocytosis professional phagocytes increase oxygen consumption (respiratory burst) through the activity of NADPH-oxidase, which generates superoxide anion (O-2(-)) and hydrogen peroxide (H2O2). We assayed the ability of A. phagocytophilum-infected neutrophils to generate O-2(-) in response to early infection (0, 3, and 5 hours) by using 2',7'-dichlorodihydrofluorescein diacetate (DCFH-DA), a fluorogenic probe commonly used to detect cellular production of reactive oxygen species (ROS). Our flow cytometric analyses showed that cell-free A. phagocytophilum induced respiratory burst 6.9-fold greater than that of LPS, an effect still evident to a lesser degree after 3 h, but absent by 5h. A. phagocytophilum initially induces and then represses respiratory burst in neutrophils. The long-term reduction in respiratory burst activity may be important for survival of A. phagocytophilum and other infectious agents in neutrophils. The effect of this may be to generate a limited functional equivalent of chronic granulomatous disease that predisposes to infections by opportunistic pathogens.