铜绿假单胞菌的LasB弹性蛋白酶与碱性蛋白酶AprA协同作用，以防止鞭毛蛋白介导的免疫识别。
The LasB Elastase of Pseudomonas aeruginosa Acts in Concert with Alkaline Protease AprA To Prevent Flagellin-Mediated Immune Recognition.
作者信息
Casilag Fiordiligie, Lorenz Anne, Krueger Jonas, Klawonn Frank, Weiss Siegfried, Häussler Susanne
机构信息
Institute for Molecular Bacteriology, Twincore-Centre for Experimental and Clinical Infection Research, a joint venture of the Helmholtz Centre for Infection Research and the Hannover Medical School, Hannover, Germany.
Institute for Molecular Bacteriology, Twincore-Centre for Experimental and Clinical Infection Research, a joint venture of the Helmholtz Centre for Infection Research and the Hannover Medical School, Hannover, Germany Department of Molecular Bacteriology, Helmholtz Centre for Infection Research, Braunschweig, Germany Department of Molecular Immunology, Helmholtz Centre for Infection Research, Braunschweig, Germany.
出版信息
Infect Immun. 2015 Oct 26;84(1):162-71. doi: 10.1128/IAI.00939-15. Print 2016 Jan.
The opportunistic pathogen Pseudomonas aeruginosa is capable of establishing severe and persistent infections in various eukaryotic hosts. It encodes a wide array of virulence factors and employs several strategies to evade immune detection. In the present study, we screened the Harvard Medical School transposon mutant library of P. aeruginosa PA14 for bacterial factors that modulate interleukin-8 responses in A549 human airway epithelial cells. We found that in addition to the previously identified alkaline protease AprA, the elastase LasB is capable of degrading exogenous flagellin under calcium-replete conditions and prevents flagellin-mediated immune recognition. Our results indicate that the production of two proteases with anti-flagellin activity provides a failsafe mechanism for P. aeruginosa to ensure the maintenance of protease-dependent immune-modulating functions.
机会致病菌铜绿假单胞菌能够在多种真核宿主中引发严重且持续的感染。它编码多种毒力因子，并采用多种策略逃避免疫检测。在本研究中，我们在铜绿假单胞菌PA14的哈佛医学院转座子突变体文库中筛选了可调节A549人呼吸道上皮细胞中白细胞介素-8反应的细菌因子。我们发现，除了先前鉴定出的碱性蛋白酶AprA外，弹性蛋白酶LasB在钙充足的条件下能够降解外源性鞭毛蛋白，并阻止鞭毛蛋白介导的免疫识别。我们的结果表明，两种具有抗鞭毛蛋白活性的蛋白酶的产生为铜绿假单胞菌提供了一种故障安全机制，以确保维持蛋白酶依赖性免疫调节功能。
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