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烧伤患者铜绿假单胞菌菌株诱导大鼠腹膜肥大细胞和人粒细胞产生炎性介质(组胺和白三烯)

Induction of inflammatory mediators (histamine and leukotrienes) from rat peritoneal mast cells and human granulocytes by Pseudomonas aeruginosa strains from burn patients.

作者信息

Bergmann U, Scheffer J, Köller M, Schönfeld W, Erbs G, Müller F E, König W

机构信息

Arbeitsgruppe für Infektabwehrmechanismen, Ruhr-Universität Bochum, Federal Republic of Germany.

出版信息

Infect Immun. 1989 Jul;57(7):2187-95. doi: 10.1128/iai.57.7.2187-2195.1989.

Abstract

Clinical isolates of Pseudomonas aeruginosa from severely burned patients were analyzed with regard to their capacity to induce inflammatory-mediator release from rat mast cells or human granulocytes. The bacterial strains were characterized according to their cell-associated hemolysin activity as well as their secreted hemolysin and phospholipase C activities. P. aeruginosa expressing heat-labile hemolysin and phospholipase C induced histamine release from rat mast cells and leukotriene formation from human granulocytes, while bacterial strains expressing heat-stable hemolysin were potent releasers of histamine but did not lead to leukotriene formation. The mediator-inducing capacity was dependent on the growth characteristics of the bacterial strains. The purified glycolipid (heat-stable hemolysin) of P. aeruginosa was a potent inducer of histamine release but did not initiate leukotriene formation. Exotoxin A did not affect inflammatory-mediator release. P. aeruginosa with leukotriene-inducing capacity also enhanced omega oxidation of endogenous leukotriene B4, suggesting an additional inactivation of the chemotactic potential. Our data suggest that both hemolysins of P. aeruginosa contribute to the pathogenicity of P. aeruginosa by inducing and modulating inflammatory-mediator release from various cells.

摘要

对严重烧伤患者的铜绿假单胞菌临床分离株进行了分析,以研究其诱导大鼠肥大细胞或人粒细胞释放炎性介质的能力。根据其细胞相关溶血素活性以及分泌的溶血素和磷脂酶C活性对细菌菌株进行了表征。表达热不稳定溶血素和磷脂酶C的铜绿假单胞菌可诱导大鼠肥大细胞释放组胺,并使人粒细胞形成白三烯,而表达热稳定溶血素的细菌菌株是组胺的有效释放剂,但不会导致白三烯形成。介质诱导能力取决于细菌菌株的生长特性。铜绿假单胞菌的纯化糖脂(热稳定溶血素)是组胺释放的有效诱导剂,但不会引发白三烯形成。外毒素A不影响炎性介质释放。具有白三烯诱导能力的铜绿假单胞菌还增强了内源性白三烯B4的ω氧化,提示趋化潜能的额外失活。我们的数据表明,铜绿假单胞菌的两种溶血素均通过诱导和调节来自各种细胞的炎性介质释放,促进了铜绿假单胞菌的致病性。

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本文引用的文献

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The virulence of Pseudomonas aeruginosa.铜绿假单胞菌的毒力。
Rev Infect Dis. 1984 Sep-Oct;6 Suppl 3:S617-26. doi: 10.1093/clinids/6.supplement_3.s617.

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