The Adh adhesin domain is required for trimeric autotransporter Apa1-mediated Actinobacillus pleuropneumoniae adhesion, autoaggregation, biofilm formation and pathogenicity
The Adh adhesin domain is required for trimeric autotransporter Apa1-mediated Actinobacillus pleuropneumoniae adhesion, autoaggregation, biofilm formation and pathogenicity
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Adh 粘附素结构域是三聚体自转运蛋白 Apa1 介导的胸膜肺炎放线杆菌粘附、自聚集、生物膜形成和致病性所必需的
DOI：
10.1016/j.vetmic.2015.02.026
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发表时间：
2015-05-15
影响因子：
3.3
通讯作者：
Lei, Liancheng
中科院分区：
文献类型：
--
作者：
Wang, Lei;Qin, Wanhai;Lei, Liancheng
胸膜肺炎放线杆菌是引起猪胸膜肺炎的病原菌，是一种高度接触性的地方病。粘连是感染过程中关键的第一步。三聚体自身转运蛋白粘附（TAAs）已被确定为新的毒力因子，但其在A.胸膜肺炎致病性在此，我们的数据表明，YadA样头区（Adh）的Apal是最佳的粘附功能域通过片段表达和粘附实验在体外。此外，Adh诱导了抗A.胸膜肺炎5 b L20和血清型1、3和5a。Adh基因的缺失显著降低了体外细胞的自聚集、生物膜形成和对宿主细胞的粘附。此外，Adh缺失株（5 b（bAdh））对仔猪的致病性显著降低，可延缓仔猪的临床症状，减少促炎细胞因子的产生，减轻感染后的肺损伤。为了阐明肺损伤的机制，本研究采用基因芯片技术和gRT-PCR技术对5 b L20和5 bcbAdh感染仔猪肺组织中差异表达基因进行了研究。与5 bL 20感染仔猪相比，5 b4）Adh感染仔猪肺组织中有495个基因表达差异（221个上调，274个下调）。特别是5 b4 Adh株感染后，抗原加工和呈递基因1F 130的表达增加。因此，Adh可能通过抑制宿主免疫识别来增强致病性。我们认为A.胸膜肺炎三聚体自身转运蛋白Apal调节自身凝集、生物膜形成、对宿主细胞的粘附和致病性。(C)2015 Elsevier B. V.版权所有。
Actinobacillus pleuropneumoniae is a causative agent of porcine pleuropneumonia, which is a highly contagious endemic disease of pigs. Adhesion is a critical first step in the infection process. Trimeric autotransporter adhesions (TAAs) have been identified as novel virulence factors; however, little is known on their roles in A. pleuropneumoniae pathogenicity. Here, our data show that YadA-like head region (Adh) of Apal was the optimal adhesion functional domain via segment expression and adhesion assays in vitro. Additionally, Adh induced partial protection against A. pleuropneumoniae 5b L20 and serotypes 1, 3, and 5a in mice. The deletion of Adh gene significantly decreased autoaggregation, biofilm formation and adherence to host cells in vitro. Furthermore, with delaying of clinical symptoms, reducing production of pro-inflammatory cytokines and lessening the lung injury after infection, Adh deletion strain (5b(bAdh) significantly reduced the pathogenicity to piglets. To elucidate the mechanism of lung injury, the differentially expressed genes in the lung tissues of piglets infected with the 5b L20 or 5bcbAdh strains were investigated using microarray analysis and validated by gRT-PCR. Compared with the 5b L20 infected piglets, 495 genes were differentially expressed in 5b4)Adh infected lung tissue (221 upregulated and 274 downregulated). Especially, the antigen processing and presentation gene 1F130 was increased following infection with the 5b4Adh strain. Thus, Adh may enhance pathogenicity by depressing host immune recognition. We conclude that the head domain of the A. pleuropneumoniae trimeric autotransporter Apal regulates autoagglutination, biofilm formation, adhesion to host cells and pathogenicity. (C) 2015 Elsevier B.V. All rights reserved.