An Actinobacillus pleuropneumoniae arcA deletion mutant is attenuated and deficient in biofilm formation
An Actinobacillus pleuropneumoniae arcA deletion mutant is attenuated and deficient in biofilm formation
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DOI：
10.1016/j.vetmic.2007.08.005
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发表时间：
2008-02-05
影响因子：
3.3
通讯作者：
Gerlach, Gerald-F.
中科院分区：
文献类型：
--
作者：
Buettner, Falk F. R.;Maas, Alexander;Gerlach, Gerald-F.
胸膜肺炎放线杆菌是猪呼吸道的兼性厌氧病原体，需要厌氧代谢活性才能在肺上皮上持久存在。研究了ArcAB双组分系统促进代谢适应厌氧环境对猪呼吸道毒力和定植的影响。使用猪感染实验，我们证明arcA的缺失呈现A。胸膜肺炎在急性感染中显著减弱，并且在未改变的肺上皮上以及在隔离中降低长期存活。与其在肠杆菌中的作用相反，arcA在A.胸膜肺炎不影响厌氧条件下的生长和存活。相反，除了亲本菌株A.胸膜肺炎Δ arcA在厌氧条件下不显示自聚集，并且缺乏生物膜形成。据推测，这些功能的缺乏是，至少在一定程度上，负责毒性的降低。(c)2007 Elsevier B.V.保留所有权利。
Actinobacillus pleuropneumoniae is a facultative anaerobic pathogen of the porcine respiratory tract requiring anaerobic metabolic activity for persistence on lung epithelium. The ArcAB two-component system facilitating metabolic adaptation to anaerobicity was investigated with regard to its impact on virulence and colonization of the porcine respiratory tract. Using pig infection experiments we demonstrate that deletion of arcA rendersA. pleuropneumoniae significantly attenuated in acute infection and reduced long-term survival on unaltered lung epithelium as well as in sequesters. Contrary to its role in enterobacteria, the deletion of arcA in A. pleuropneumoniae does not affect growth and survival under anaerobic conditions. Instead, other than the parent strain A. pleuropneumoniae Delta arcA does not show autoaggregation under anaerobic conditions and is deficient in biofilm formation. It is hypothesized that the lack of these functions is, at least in part, responsible for the reduction of virulence. (c) 2007 Elsevier B.V. All rights reserved.