Autoinducer 2 is required for Biofilm growth of Aggregatibacter (Actinobacillus) actinomycetemcomitans
Autoinducer 2 is required for Biofilm growth of Aggregatibacter (Actinobacillus) actinomycetemcomitans
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DOI：
10.1128/iai.00402-07
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发表时间：
2007-09-01
影响因子：
3.1
通讯作者：
Demuth, Donald R.
中科院分区：
文献类型：
--
作者：
Shao, Hanjuan;Lamont, Richard J.;Demuth, Donald R.
在铁限制条件下，伴放线放线杆菌的生长需要自身诱导物2（AI-2）。然而，在体内，这种生物体在人类口腔中形成的复杂的多物种生物膜中茁壮成长。在这份报告中，我们表明，粘附生长的A。放线菌共生体的唾液涂覆的表面上，但不是在充满铁的条件下的共生生长，是有缺陷的LuxS-缺乏的背景。生物膜生长的luxS突变体表现出较低的总生物量和较低的生物膜深度比野生型菌株。正常的生物膜生长的luxS突变体恢复遗传的luxS的功能性拷贝的引入和生物化学通过添加部分纯化的AI-2。此外，将S-腺苷高半胱氨酸水解酶导入A.这表明AI-2本身是放线菌共生菌生物膜生长所必需的。放线菌当编码AI-2相互作用蛋白RbsB或LsrB的基因失活时，也观察到类似于LuxS缺陷型菌株的生物膜生长缺陷。生物膜的形成。在rbsB和IsrB两者失活后，几乎消除了伴放线菌。此外，野生型A.在核糖的存在下，放线菌共生菌的活性降低，核糖与AI-2竞争结合RbsB。这些结果表明，RbsB和LsrB在A. actinomycetemcomitans和A.放线菌共生菌生物膜需要AI-2。
Autoinducer 2 (AI-2) is required for the growth of Aggregatibacter (Actinobacillus) actinomycetentcomitans in culture under conditions of iron limitation. However, in vivo this organism thrives in a complex multispecies biofilm that forms in the human oral cavity. In this report, we show that adherent growth of A. actinomycetemcomitans on a saliva-coated surface, but not planktonic growth under iron-replete conditions, is defective in a LuxS-deficient background. Biofilm growth of the luxS mutant exhibited lower total biomass and lower biofilm depth than those for the wild-type strain. Normal biofilm growth of the luxS mutant was restored genetically by introduction of a functional copy of luxS and biochemically by addition of partially purified AI-2. Furthermore, introduction of S-adenosylhomocysteine hydrolase, which restores the metabolism of S-adenosylmethionine in the absence of LuxS, into A. actinomycetemcomitans did not complement the luxS mutation unless AI-2 was added in trans. This suggests that AI-2 itself is required for biofilm growth by A. actinomycetemeomitans. A biofilm growth deficiency similar to that of the LuxS-deficient strain was also observed when a gene encoding the AI-2-interacting protein RbsB or LsrB was inactivated. Biofilm formation by A. actinomycetemcomitans was virtually eliminated upon inactivation of both rbsB and IsrB. In addition, biofilm growth by wild-type A. actinomycetemcomitans was reduced in the presence of ribose, which competes with AI-2 for binding to RbsB. These results suggest that RbsB and LsrB function as AI-2 receptors in A. actinomycetemcomitans and that the development of A. actinomycetemcomitans biofilms requires AI-2.