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首页> 外文期刊>Microbial Pathogenesis >High levels of nitric oxide production decrease early but increase late survival of Brucella abortus in macrophages
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High levels of nitric oxide production decrease early but increase late survival of Brucella abortus in macrophages

机译：一氧化氮的高水平生产可减少巨噬细胞中流产布鲁氏菌的早期存活，但增加晚期存活

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摘要

Nitric oxide (NO), produced by the NOS protein, is known as a defense mechanism against various pathogens and an apoptotic inducer of cells. Apoptosis can also be a host protective mechanism against intracellular bacteria. The intracellular survival of Brucella abortus in RAW264.7 macrophages was examined under conditions of the apoptotic inducer, NO. Since B. abortus does not induce high output of NO, Escherichia coli LPS and IFN-gamma, as potential therapeutic modalities, were added to increase the expression of NOS, and thus NO. Using 10 ng/ml E coli LPS and 25 U/ml IFN-gamma, nitrite production was as high as 140 muM by 72 h. However, when macrophages were infected with B. abortus, the nitrite concentration was 60 muM after 72 h post infection, greater than a two-fold decrease. The number of surviving bacteria decreased, from 6 to 24 h, in the presence of nitrite accumulation. In the absence of B. abortus there was an increase in apoptotic cells at 72 h with high nitrite accumulation. In contrast, the number of macrophage apoptotic bodies decreased in the presence of B. abortus. The data suggest that: (i) NO accelerates the killing of intracellular B. abortus, but not to completion during the first 24 h of infection; (ii) B. abortus can prevent apoptosis as an advantage for bacterial survival inside macrophages and (iii) surviving intracellular bacteria then replicate steadily after 24 h. B. abortus probably expresses genes that counteract the effect of a high NO environment or activates genes to utilize NO as a nitrogen source, as the Brucella genome codes for nitric and nitrous oxide reductase genes.
机译：由NOS蛋白产生的一氧化氮（NO）被称为抵抗各种病原体和细胞凋亡诱导剂的防御机制。凋亡也可以是针对细胞内细菌的宿主保护机制。在凋亡诱导物NO的条件下检查了RAW264.7巨噬细胞中布鲁氏菌流产的细胞内存活。由于流产双歧杆菌不会诱导NO的高输出，因此添加了作为潜在治疗手段的大肠杆菌LPS和IFN-γ来增加NOS的表达，从而增加NO的表达。使用10 ng / ml大肠杆菌LPS和25 U / mlIFN​​-γ，到72小时亚硝酸盐产量高达140μM。但是，当巨噬细胞感染了流产双歧杆菌后，感染后72小时亚硝酸盐浓度为60μM，下降幅度超过两倍。在亚硝酸盐积累的情况下，存活细菌的数量从6小时减少到24小时。在不存在流产芽孢杆菌的情况下，在72 h时凋亡细胞增加，亚硝酸盐积累高。相反，在流产双歧杆菌存在下，巨噬细胞凋亡小体的数量减少。数据表明：（i）NO加速了杀灭细胞内流产双歧杆菌的能力，但在感染的最初24小时内并未完全杀灭; （ii）流产芽孢杆菌可防止凋亡，这是巨噬细胞内部细菌存活的优势，并且（iii）存活的细胞内细菌可在24小时后稳定复制。流产芽孢杆菌可能表达抵消高NO环境影响的基因或激活基因以利用NO作为氮源，因为布鲁氏菌基因组编码一氧化氮和一氧化二氮还原酶基因。

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