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首页> 外文期刊>Journal of Leukocyte Biology: An Official Publication of the Reticuloendothelial Society >Urokinase-deficient and urokinase receptor-deficient mice have impaired neutrophil antimicrobial activation in vitro.
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Urokinase-deficient and urokinase receptor-deficient mice have impaired neutrophil antimicrobial activation in vitro.

机译：尿激酶不足和尿激酶受体不足的小鼠在体外损害了中性粒细胞的抗菌活性。

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摘要

Leukocytes express both urokinase-type plasminogen activator (uPA) and the urokinase receptor (uPAR, CD87). We have shown that neutrophil recruitment to the lung during P. aeruginosa pneumonia is impaired in uPAR-deficient (uPAR-/-) mice but is normal in uPA-/- mice. However, both uPA-/- mice and uPAR-/- mice have impaired lung clearance of P. aeruginosa compared with wild-type (WT) mice. To determine the role of uPA and uPAR in antibacterial host defense, we compared neutrophil bacterial-phagocytosis, respiratory burst, and degranulation among uPA-/-, uPAR-/-, and WT mice. Neutrophil phagocytosis was significantly diminished comparing uPA-/- and uPAR-/- mice with WT mice at all time points. The generation of superoxide by both uPA-/- and uPAR-/- neutrophils was about half of that seen in WT neutrophils. Degranulation of azurophilic granules was significantly diminished in uPA-/- neutrophils compared with either uPAR-/- or WT neutrophils. By contrast, agonist-stimulated release of specific granules wasnot diminished in either uPA-/- or uPAR-/- mice compared with WT. We conclude that the uPA/uPAR system modulates several of the crucial steps in neutrophil activation that result in bacterial killing and effective innate host defense.
机译：白细胞同时表达尿激酶型纤溶酶原激活物（uPA）和尿激酶受体（uPAR，CD87）。我们已经表明，在uPAR缺乏（uPAR-/-）小鼠中，铜绿假单胞菌肺炎期间中性粒细胞向肺的募集受到损害，但在uPA-/-小鼠中却是正常的。但是，与野生型（WT）小鼠相比，uPA-/-小鼠和uPAR-/-小鼠均损害了铜绿假单胞菌的肺部清除能力。为了确定uPA和uPAR在抗菌宿主防御中的作用，我们比较了uPA-/-，uPAR-/-和WT小鼠之间的嗜中性粒细胞吞噬作用，呼吸爆发和脱粒。在所有时间点，将uPA-/-和uPAR-/-小鼠与WT小鼠相比，嗜中性粒细胞的吞噬作用显着降低。 uPA-/-和uPAR-/-中性粒细胞产生的超氧化物约为WT中性粒细胞产生的一半。与uPAR-/-或WT中性粒细胞相比，uPA-/-中性粒细胞中的嗜酸性颗粒的去粒作用明显减少。相反，与WT相比，uPA-/-或uPAR-/-小鼠中激动剂刺激的特定颗粒的释放没有减少。我们得出的结论是，uPA / uPAR系统调节嗜中性粒细胞活化中的几个关键步骤，从而导致细菌杀伤和有效的先天宿主防御。

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