The role of Pseudomonas aeruginosa elastase as a potent inflammatory factor in a rat air pouch inflammation model.
The role of Pseudomonas aeruginosa elastase as a potent inflammatory factor in a rat air pouch inflammation model.
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DOI：
10.1111/j.1574-695x.1999.tb01356.x
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发表时间：
1999-08
影响因子：
--
通讯作者：
Y. Kon;H. Tsukada;T. Hasegawa;K. Igarashi;K. Wada;E. Suzuki;M. Arakawa;F. Gejyo
中科院分区：
文献类型：
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作者：
Y. Kon;H. Tsukada;T. Hasegawa;K. Igarashi;K. Wada;E. Suzuki;M. Arakawa;F. Gejyo
铜绿假单胞菌是一种机会性病原体，可在患有基础呼吸道疾病(如支气管扩张、囊性纤维化和弥漫性泛细支气管炎)的患者中导致危及生命的感染。大多数铜绿假单胞菌在宿主的感染状态下会产生某种具有广泛底物特异性的蛋白酶。铜绿假单胞菌弹性蛋白酶是最强的外毒素之一，具有组织损伤蛋白分解活性，能够降解免疫球蛋白、补体因子和细胞因子等血浆蛋白。本研究旨在探讨铜绿假单胞菌弹性蛋白酶在宿主炎症反应中对炎症部位中性粒细胞聚集的影响。采用大鼠气囊模型，分析气囊腔内注射铜绿假单胞菌弹性酶后白细胞数、渗出液体积和白介素8浓度的变化。中性粒细胞数量和囊腔渗出液体积在4h显著增加，8h达高峰，呈剂量依赖关系，随后下降，IL-8浓度比中性粒细胞高峰提前4h达到峰值。铜绿假单胞菌弹性蛋白酶的活性似乎加强了炎症过程。脂多糖污染的影响可以忽略不计。虽然这些观察是在皮下腔内进行的，但它们表明铜绿假单胞菌弹性蛋白酶在感染铜绿假单胞菌的病例中作为免疫刺激因子在炎症反应中发挥作用。
Pseudomonas aeruginosa, an opportunistic pathogen, can cause life threatening infections in patients compromised by underlying respiratory disease like bronchiectasis, cystic fibrosis and diffuse panbronchiolitis. Most strains of P. aeruginosa produce some kind of protease with broad substrate specificities during the infectious state in the host. P. aeruginosa elastase, one of the strongest exotoxins, has a tissue-damaging proteolytic activity and is capable of degrading such plasma proteins as immunoglobulins, complement factor and cytokines. The present study focused on the effect of P. aeruginosa elastase and was designed to evaluate the neutrophil accumulation at the inflammation site mediated by P. aeruginosa elastase in the inflammatory response in the host. An air pouch model in rats, considered as a useful model of inflammation, was used to analyze the number of leukocytes, the volume of exudate and the concentration of interleukin-8 after the injection of P. aeruginosa elastase into the pouch cavity. The number of neutrophils and the volume of exudate in the pouch cavity increased significantly at 4 h, peaked at 8 h in a dose-dependent manner and then decreased at 24 h. The concentration of interleukin-8 in pouch fluid peaked 4 h earlier than the peak of the neutrophil number. The enzymatic activity of P. aeruginosa elastase seemed to reinforce the inflammation process. The influence of lipopolysaccharide contamination was negligible. Although these observations were made in the subcutaneous cavity, they indicate that P. aeruginosa elastase plays a role as an immunoprovocative factor in the inflammatory response in cases of infection with P. aeruginosa.