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首页> 外文期刊>Infection and immunity >Autoinducer-2 and QseC Control Biofilm Formation and In Vivo Virulence of Aggregatibacter actinomycetemcomitans
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Autoinducer-2 and QseC Control Biofilm Formation and In Vivo Virulence of Aggregatibacter actinomycetemcomitans

机译：Autoinducer-2和QseC控制生物膜的形成和聚集性放线菌的体内毒力

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Biofilm formation by the periodontal pathogen Aggregatibacter actinomycetemcomitans is dependent upon autoinducer-2 (AI-2)-mediated quorum sensing. However, the components that link the detection of the AI-2 signal to downstream gene expression have not been determined. One potential regulator is the QseBC two-component system, which is part of the AI-2-dependent response pathway that controls biofilm formation in Escherichia coli. Here we show that the expression of QseBC in A. actinomycetemcomitans is induced by AI-2 and that induction requires the AI-2 receptors, LsrB and/or RbsB. Additionally, inactivation of qseC resulted in reduced biofilm growth. Since the ability to grow in biofilms is essential for A. actinomycetemcomitans virulence, strains that were deficient in QseC or the AI-2 receptors were examined in an in vivo mouse model of periodontitis. The ΔqseC mutant induced significantly less alveolar bone resorption than the wild-type strain (P < 0.02). Bone loss in animals infected with the ΔqseC strain was similar to that in sham-infected animals. The ΔlsrB, ΔrbsB, and ΔlsrB ΔrbsB strains also induced significantly less alveolar bone resorption than the wild type (P < 0.03, P < 0.02, and P < 0.01, respectively). However, bone loss induced by a ΔluxS strain was indistinguishable from that induced by the wild type, suggesting that AI-2 produced by indigenous microflora in the murine oral cavity may complement the ΔluxS mutation. Together, these results suggest that the QseBC two-component system is part of the AI-2 regulon and may link the detection of AI-2 to the regulation of downstream cellular processes that are involved in biofilm formation and virulence of A. actinomycetemcomitans.
机译：牙周病原体 Agactibacteractinomycetemcomitans 的生物膜形成取决于autoinducer-2（AI-2）介导的群体感应。但是，尚未确定将AI-2信号的检测与下游基因表达相关联的组件。一种潜在的调节剂是QseBC两组分系统，它是AI-2依赖反应途径的一部分，该途径控制大肠杆菌中的生物膜形成。在这里，我们证明了QseBC在 A中的表达。放线放线菌是由AI-2诱导的，该诱导需要AI-2受体LsrB和/或RbsB。此外， qseC 的失活导致生物膜生长减少。由于生物膜的生长能力对于 A是必不可少的。在牙周炎的体内小鼠模型中检查了放线菌的致病力，QseC或AI-2受体缺陷的菌株。 Δ qseC 突变体引起的牙槽骨吸收明显低于野生型菌株（ P <0.02）。用Δ qseC 菌株感染的动物的骨丢失与假感染动物相似。 Δ lsrB ，Δ rbsB 和Δ lsrB Δ rbsB 菌株引起的牙槽骨吸收也明显少于野生型（ P <0.03， P <0.02和 P <0.01）。然而，Δ luxS 菌株引起的骨丢失与野生型没有明显区别，这表明小鼠口腔中原生菌群产生的AI-2可以补充Δ luxS < / em>突变。总之，这些结果表明QseBC两组分系统是AI-2调节剂的一部分，并且可能将AI-2的检测与下游细胞过程的调控联系起来，这些过程与生物膜形成和 A的毒力有关。放线菌。

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