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首页> 外文期刊>Infection and immunity >Pseudomonas aeruginosa alginate in cystic fibrosis sputum and the inflammatory response.
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Pseudomonas aeruginosa alginate in cystic fibrosis sputum and the inflammatory response.

机译：铜绿假单胞菌藻酸盐在囊性纤维化痰中的炎症反应。

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Alginate, a viscous polysaccharide from mucoid Pseudomonas aeruginosa, may interfere with the host defenses in patients with cystic fibrosis and chronic P. aeruginosa lung infection. The alginate concentration in the sol phase of expectorated sputum was quantitated by a biochemical method and a newly developed enzyme-linked immunosorbent assay. There was a high degree of correlation between the methods, and the concentration of alginate ranged from 4 to 101 micrograms/ml with a median of 35.5 micrograms/ml when measured by enzyme-linked immunosorbent assay. Alginate could not be detected in the bronchial secretions from patients without P. aeruginosa infection. In vitro investigation of alginate did not show any activation of the alternative pathway of complement, as determined by a hemolytic kinetic assay and by testing for neutrophil chemotaxis. At a high concentration, P. aeruginosa alginate caused a slight activation of the classical pathway of complement. Alginate did not cause neutrophil chemotaxis by itself but was able to reduce the neutrophil chemotactic response to N-formylmethionylleucylphenylalanine and for zymosan-activated serum. P. aeruginosa and seaweed alginates were able to prime neutrophils for increased N-formylmethionylleucylphenylalanine-induced neutrophil oxidative burst, as determined by chemiluminescence. Because of its ability to prevent attraction of neutrophils to the site of infection, lack of complement activation, and ability to enhance neutrophil oxidative burst, alginate from P. aeruginosa may contribute to the persistence and pathogenesis of chronic P. aeruginosa infection in cystic fibrosis.
机译：海藻酸钠是粘液状铜绿假单胞菌的粘性多糖，可能会干扰患有囊性纤维化和慢性铜绿假单胞菌肺部感染的患者的宿主防御。通过生化方法和新开发的酶联免疫吸附测定法定量化痰痰中溶胶相中的藻酸盐浓度。这些方法之间存在高度相关性，通过酶联免疫吸附测定法测得的藻酸盐浓度范围为4至101微克/毫升，中位数为35.5微克/毫升。没有铜绿假单胞菌感染的患者的支气管分泌物中未检测到藻酸盐。通过溶血动力学测定和嗜中性粒细胞趋化性测试确定，藻酸盐的体外研究未显示补体替代途径的任何激活。在高浓度下，铜绿假单胞菌藻酸盐引起经典补体途径的轻微激活。海藻酸盐本身不会引起嗜中性粒细胞趋化性，但能够降低嗜中性粒细胞对N-甲酰基甲硫酰基亮氨酰苯丙氨酸和酵母聚糖活化血清的趋化性反应。铜绿假单胞菌和海​​藻藻酸盐能够引发嗜中性粒细胞，以增加N-甲酰基甲硫酰基亮氨酰苯基丙氨酸诱导的嗜中性粒细胞的氧化爆发，如化学发光法所确定。由于铜绿假单胞菌的藻酸盐具有防止嗜中性白细胞吸引到感染部位的能力，缺乏补体激活和增强嗜中性粒细胞氧化爆发的能力，因此可能有助于慢性铜绿假单胞菌感染在囊性纤维化中的持久性和发病机理。

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