Biological effects of Pseudomonas aeruginosa phenazine pigments.
Biological effects of Pseudomonas aeruginosa phenazine pigments.
复制标题
铜绿假单胞菌吩嗪色素的生物学效应。
DOI：
10.1159/000414339
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发表时间：
1987
期刊：
影响因子：
--
通讯作者：
Klinger,JD
中科院分区：
文献类型：
--
作者：
Sorensen,RU;Klinger,JD
吩嗪色素的产生是铜绿假单胞菌的一个显著特征，尽管其他微生物，包括洋葱假单胞菌，也是这些代谢物的天然来源[1，2]。其中一种颜料，pyridine（1-羟基-5-甲基-吩嗪），由于其抗菌特性而被广泛研究[1-3]。脓毒症的潜在致病作用是有争议的。1941年，Schoental [4]发现50 mg/ml的浓度抑制培养的成纤维细胞的生长，腹腔注射2 mg的吡奥苏胺对小鼠是致命的。随后的研究未能揭示体内毒性[5，6]，导致刘[7]得出结论，脓毒症在人类感染的发病机制中不起作用。然而，脓毒症已被证明在几个系统中改变细胞功能。它增强需要有氧糖酵解的组织的呼吸[8]，并抑制小鼠单核细胞[9]、HeLa细胞[10]、分离的小鼠肝线粒体[11，12]、培养的BHK细胞和完整的豚鼠腹腔巨噬细胞[13]对分子氧的摄取。我们开始对脓毒症在铜绿假单胞菌及其上清液在淋巴细胞培养物中的细胞抑制作用中的作用感兴趣，假设这种作用可能有助于慢性铜绿假单胞菌感染部位的局部免疫抑制机制[14，15]。在下面的讨论中，我们
The production of phenazine pigments is a distinctive feature of Pseu-domonas aeruginosa, although other microorganisms, including Pseudo-monas cepacia, are also natural sources of some of these metabolites [1, 2]. One of these pigments, pyocyanine (1-hydroxy-5-methyl-phenazine), has been extensively studied because of its antibiotic properties [1-3]. The potential pathogenic role of pyocyanine is controversial. In 1941, Schoental [4] found that concentrations of 50 mg/ml inhibited the growth of cultured fibroblasts, and intraperitoneal injections of 2 mg of pyосуаnine were lethal for mice. Subsequent studies failed to reveal toxicity in vivo [5, 6], leading Liu [7] to conclude that pyocyanine plays no part in the pathogenesis of human infections.Nevertheless, pyocyanine has been shown to alter cell functions in several systems. It enhances the respiration of tissues that require aerobic glycolysis [8] and inhibits the uptake of molecular oxygen by mouse monocytes [9], HeLa cells [10], isolated mouse liver mitochondria [11, 12], cul-tured BHK cells, and intact guinea pig peritoneal macrophages [13]. We became interested in the role of pyocyanine in the cytostatic effect of P. aeruginosa and its supernatants in lymphocyte cultures, postulating that this effect may contribute to local immunosuppressive mechanisms at sites of chronic P. aeruginosa infection [14, 15]. In the following discussion, we