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首页> 外文期刊>BMC Genomics >Quorum sensing of Streptococcus mutans is activated by Aggregatibacter actinomycetemcomitans and by the periodontal microbiome
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Quorum sensing of Streptococcus mutans is activated by Aggregatibacter actinomycetemcomitans and by the periodontal microbiome

机译:变形链球菌的群体感应通过聚合放线菌和结节菌激活

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Background The oral cavity is inhabited by complex microbial communities forming biofilms that can cause caries and periodontitis. Cell-cell communication might play an important role in modulating the physiologies of individual species, but evidence so far is limited. Results Here we demonstrate that a pathogen of the oral cavity, Aggregatibacter actinomycetemcomitans ( A. act. ), triggers expression of the quorum sensing (QS) regulon of Streptococcus mutans, a well-studied model organism for cariogenic streptococci, in dual-species biofilms grown on artificial saliva. The gene for the synthesis of the QS signal XIP is essential for this interaction. Transcriptome sequencing of biofilms revealed that S. mutans up-regulated the complete QS regulon (transformasome and mutacins) in the presence of A. act . and down-regulated oxidative stress related genes. A.act . required the presence of S. mutans for growth. Fimbriae and toxins were its most highly expressed genes and up-regulation of anaerobic metabolism, chaperones and iron acquisition genes was observed in co-culture. Metatranscriptomes from periodontal pockets showed highly variable levels of S. mutans and low levels of A. act. . Transcripts of the alternative sigma-factor SigX, the key regulator of QS in S. mutans , were significantly enriched in periodontal pockets compared to single cultures (log2 4.159, FDR?≤0.001, and expression of mutacin related genes and transformasome components could be detected. Conclusion The data show that the complete QS regulon of S. mutans can be induced by an unrelated oral pathogen and S. mutans may be competent in oral biofilms in vivo.
机译:背景技术口腔中居住着复杂的微生物群落,形成了可引起龋齿和牙周炎的生物膜。细胞间通讯可能在调节单个物种的生理过程中起重要作用,但到目前为止,证据还很有限。结果在这里,我们证明了口腔病原体,放线杆菌(A. act。),在双物种生物膜中触发了变形链球菌的群体感应(QS)基因组的表达,变形链球菌是一种经过深入研究的致龋性链球菌模型生物。生长在人工唾液上。 QS信号XIP的合成基因对于这种相互作用至关重要。生物膜的转录组测序表明,变形链球菌在A. act的存在下上调了完整的QS调节子(transformasome和mutacins)。和下调氧化应激相关基因。行动需要存在变形链球菌才能生长。菌毛和毒素是其最高表达的基因,在共培养中观察到厌氧代谢,伴侣蛋白和铁获取基因的上调。来自牙周袋的元转录组显示变异链球菌水平高度可变,而拟链球菌水平较低。 。与单一培养物相比,替代sigma因子SigX(变异链球菌中QS的关键调控因子)的转录本在牙周袋中显着富集(log 2 4.159,FDR?≤0.001和突变蛋白的表达)结论变形链球菌的完整QS调控可被无关的口腔病原菌诱导,变形链球菌可能在口腔生物膜中发挥作用。

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