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首页> 外文期刊>American Journal of Physiology >Role of PAR2 in murine pulmonary pseudomonal infection
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Role of PAR2 in murine pulmonary pseudomonal infection

机译：PAR2在鼠肺假单胞菌感染中的作用

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First published December 14, 2007; doi:10.1152/ajplung.00036.2007.-Proteinases can influence lung inflammation by various mechanisms, including via cleavage and activation of protease-activated receptors (PAR) such as PAR2. In addition, proteinases such as neutrophil and/or Pseudonwnas-dtrived elastase can disarm PAR2 resulting in loss of PAR2 signaling. Currently, the role of PAR2 in host defense against bacterial infection is not known. Using a murine model of acute Pseudomonas aeruginosa pneumonia, we examined differences in the pulmonary inflammatory response between wild-type and PAR2~(-/-) mice. Compared with wild-type mice, PAR2~(-/-) mice displayed more severe lung inflammation and injury in response to P. aeruginosa infection as indicated by higher bronchoalveolar lavage fluid neutrophil numbers, protein concentration, and TNF-alpha levels. By contrast, IFN-7 levels were markedly reduced in PAR2 compared with wild-type mice. Importantly, clearance of P. aeruginosa was diminished in PAR2~(-/-) mice. In vitro testing revealed that PAR2 neutrophils killed significantly less bacteria than wild-type murine neutrophils. Further, both neutrophils and macrophages from PAR2 mice displayed significantly reduced phagocytic efficiency compared with wild-type phagocytes. Stimulation of PAR2 on macrophages using a PAR2-activating peptide resulted in enhanced phagocytosis directly implicating PAR2 signaling in the phagocytic process. We conclude that genetic deletion of PAR2 is associated with decreased clearance of P. aeruginosa. Our data suggest that a deficiency in IFN-y production and impaired bacterial phagocytosis are two potential mechanisms responsible for this defect.
机译：首次发布于2007年12月14日; doi：10.1152 / ajplung.00036.2007.-蛋白酶可以通过多种机制影响肺部炎症，包括通过裂解和激活蛋白酶激活受体（PAR）（例如PAR2）。另外，诸如嗜中性粒细胞和/或假单胞菌提取的弹性蛋白酶的蛋白酶可以使PAR2解除武装，从而导致PAR2信号传导的丧失。目前，尚不知道PAR2在宿主抵抗细菌感染的防御中的作用。使用急性铜绿假单胞菌肺炎的小鼠模型，我们检查了野生型和PAR2〜（-/-）小鼠之间肺部炎症反应的差异。与野生型小鼠相比，PAR2〜（-/-）小鼠表现出对铜绿假单胞菌感染更严重的肺部炎症和损伤，这表现为更高的支气管肺泡灌洗液中性粒细胞数量，蛋白质浓度和TNF-α水平。相比之下，与野生型小鼠相比，PAR2中的IFN-7水平显着降低。重要的是，在PAR2〜（-/-）小鼠中铜绿假单胞菌的清除减少了。体外测试显示，PAR2中性粒细胞杀死的细菌比野生型鼠中性粒细胞少得多。此外，与野生型吞噬细胞相比，来自PAR2小鼠的嗜中性粒细胞和巨噬细胞均显示出吞噬效率显着降低。使用激活PAR2的肽刺激巨噬细胞上的PAR2导致吞噬作用增强，直接将PAR2信号传导牵连在吞噬过程中。我们得出结论，PAR2的基因删除与铜绿假单胞菌的清除率降低相关。我们的数据表明，IFN-γ产生缺乏和细菌吞噬功能受损是造成该缺陷的两个潜在机制。

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