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首页> 外文期刊>Infection and immunity >Pseudomonas aeruginosa selective adherence to and entry into human endothelial cells.
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Pseudomonas aeruginosa selective adherence to and entry into human endothelial cells.

机译：铜绿假单胞菌对人内皮细胞的选择性粘附和进入。

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The pathogenesis of Pseudomonas aeruginosa disseminated infections depends on bacterial interaction with blood vessels. We have hypothesized that in order to traverse the endothelial barrier, bacteria would have to adhere to and damage endothelial cells. To test this hypothesis, we studied the adherence to human endothelial cells in primary culture of the piliated P. aeruginosa strain PAK and of two isogenic nonpiliated strains: PAK/p-, which carries a mutation in the pilin structural gene, and PAK-N1, a mutant defective in the regulatory rpoN gene. PAK adhered significantly more than did the pilus-lacking strains. P. aeruginosa was also taken up by endothelial cells, as determined by quantitative bacteriologic assays and by transmission electron microscopy. This internalization of P. aeruginosa seems to be a selective process, since the piliated strain was taken up significantly more than the nonpiliated bacteria and the avirulent Escherichia coli DH5 alpha, even following bacterial centrifugation onto the cell monolayers. A significant fraction of the internalized P. aeruginosa PAK was recovered in a viable form after 6 h of residence within endothelial cells. Progressive endothelial cell damage resulted from PAK intracellular harboring, as indicated by the release of lactate dehydrogenase. An increasing concentration of PAK cells was recovered from the extracellular medium with time, suggesting that ingested bacteria were released from endothelial cells and multiplied freely. We speculate that in vivo the ability of some P. aeruginosa strains to resist intracellular residence would afford protection from host defenses and antibiotics and that the release of viable bacteria into bloodstream may represent a central feature of the pathogenesis of bacteremia in compromised patients.
机译：铜绿假单胞菌传播感染的发病机理取决于细菌与血管的相互作用。我们假设，为了穿越内皮屏障，细菌必须粘附并破坏内皮细胞。为了验证这一假设，我们研究了铜绿假单胞菌PAK菌株和两个同基因非软化菌株：PAK / p-（在菌毛结构基因中携带突变）和PAK-N1在原代培养物中对人内皮细胞的粘附性，这是调节性rpoN基因缺陷的突变体。 PAK的粘附力明显强于缺乏菌毛的菌株。铜绿假单胞菌也被内皮细胞吸收，这是通过定量细菌学测定和透射电子显微镜确定的。铜绿假单胞菌的这种内在化似乎是一个选择性的过程，因为即使在细菌离心到细胞单层之后，菌丝体的吸收也比未菌丝的细菌和无毒大肠杆菌DH5α吸收得多。在内皮细胞内停留6小时后，以可行的形式回收了很大一部分内化的铜绿假单胞菌PAK。乳酸脱氢酶的释放表明，PAK的细胞内窝藏导致了进行性内皮细胞损伤。随着时间的推移，从细胞外培养基中回收到的PAK细胞浓度不断增加，这表明摄入的细菌从内皮细胞中释放出来并自由繁殖。我们推测，在体内某些铜绿假单胞菌菌株抵抗细胞内滞留的能力将提供对宿主防御和抗生素的保护作用，并且活菌向血液中的释放可能代表了受感染患者菌血症发病机理的主要特征。

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