Inactivation of human bronchial mucosal proteinase inhibitor by Pseudomonas aeruginosa elastase.
Inactivation of human bronchial mucosal proteinase inhibitor by Pseudomonas aeruginosa elastase.
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铜绿假单胞菌弹性蛋白酶灭活人支气管粘膜蛋白酶抑制剂。
DOI：
10.1164/arrd.1982.126.6.1070
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发表时间：
1982
期刊：
影响因子：
--
通讯作者：
W. Dralle
中科院分区：
文献类型：
--
作者：
D. Johnson;B. Carter;W. Dralle
人支气管粘液含有一种称为支气管粘液抑制剂（BMI）的酸稳定蛋白酶抑制剂，其明显地保护上呼吸道免受多形白细胞（PMN）弹性蛋白酶和组织蛋白酶G的蛋白水解，并且也产生弹性蛋白酶的铜绿假单胞菌的感染可导致相当大的肺损伤。研究了BMI在铜绿假单胞菌弹性蛋白酶（一种锌金属蛋白酶）存在下保护肺免受蛋白水解攻击的可能作用。BMI不仅不能抑制铜绿假单胞菌弹性蛋白酶，而且在细菌弹性蛋白酶存在下，BMI抑制PMN弹性蛋白酶和组织蛋白酶G的能力迅速丧失。铜绿假单胞菌弹性蛋白酶还从与BMI的复合物中释放活性PMN弹性蛋白酶，导致弹性蛋白被两种酶消化。在铜绿假单胞菌感染中观察到的肺组织蛋白质水解可能是由细菌和中性粒细胞蛋白酶的组合引起的。从白细胞释放的弹性蛋白酶和组织蛋白酶G被吸引到铜绿假单胞菌感染部位，在BMI被铜绿假单胞菌弹性蛋白酶灭活后将自由地攻击支气管组织，增加了由细菌蛋白酶引起的损伤。
Human bronchial mucus contains an acid-stable proteinase inhibitor called bronchial mucous inhibitor (BMI) that apparently protects the upper airways from proteolysis by polymorphonuclear leukocyte (PMN) elastase and cathepsin G, and infections of Pseudomonas aeruginosa, which also produces an elastase, can result in considerable lung damage. The possible role of BMI in protecting the lung from proteolytic attack in the presence of P. aeruginosa elastase (a zinc metalloprotease) was investigated. The BMI not only failed to inhibit P. aeruginosa elastase but the ability of BMI to inhibit PMN elastase and cathepsin G was rapidly lost in the presence of the bacterial elastase. The P. aeruginosa elastase also freed active PMN elastase from complexes with BMI, resulting in elastin digestion by both enzymes. The proteolysis of lung tissue observed with P. aeruginosa infections may be caused by a combination of bacterial and PMN proteases. Elastase and cathepsin G released from leukocytes, attracted to P. aeruginosa infection sites, would be free to attack the bronchial tissues after BMI inactivation by P. aeruginosa elastase, adding to the damage caused by the bacterial protease(s).