Direct interactions with commensal streptococci modify intercellular communication behaviors of Streptococcus mutans.
Direct interactions with commensal streptococci modify intercellular communication behaviors of Streptococcus mutans.
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与共生链球菌的直接相互作用改变了变形链球菌的细胞间通讯行为。
DOI：
10.1038/s41396-020-00789-7
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发表时间：
2021-03
期刊：
影响因子：
--
通讯作者：
Burne RA
中科院分区：
文献类型：
--
作者：
Kaspar JR;Lee K;Richard B;Walker AR;Burne RA
龋齿的形成是一个复杂的过程，最终导致牙釉质被附着的生物膜中的微生物产生的酸破坏。在这些生物膜内发生的致龋细菌（如变形链球菌）和与健康相关的链球菌之间的细菌相互作用被认为是健康和疾病的关键决定因素。为了更好地理解这些相互作用，将通过肽信号传导主动监测细胞-细胞通信的变形链球菌报告菌株与不同的链球菌共培养。信号S。变形链球菌通常在单一培养物中高度活跃，但仅当细菌与S.变异人我们发现了一个新的基因表达模式，发生在S。当直接与这些细菌一起培养时，最后，缺乏先前显示的拮抗基因产物的突变体衍生物在共培养物中显示野生型水平的信号抑制。总的来说，这些结果揭示了多种健康相关链球菌中的一种新途径，该途径阻断肽信号传导并诱导S.变异体了解这种抑制作用的分子基础将有助于合理设计针对最普遍的口腔传染病的新风险评估、诊断和治疗方法。
The formation of dental caries is a complex process that ultimately leads to damage of the tooth enamel from acids produced by microbes in attached biofilms. The bacterial interactions occurring within these biofilms between cariogenic bacteria, such as the mutans streptococci, and health-associated commensal streptococci, are thought to be critical determinants of health and disease. To better understand these interactions, a Streptococcus mutans reporter strain that actively monitors cell–cell communication via peptide signaling was cocultured with different commensal streptococci. Signaling by S. mutans, normally highly active in monoculture, was completely inhibited by several species of commensals, but only when the bacteria were in direct contact with S. mutans. We identified a novel gene expression pattern that occurred in S. mutans when cultured directly with these commensals. Finally, mutant derivatives of commensals lacking previously shown antagonistic gene products displayed wild-type levels of signal inhibition in cocultures. Collectively, these results reveal a novel pathway(s) in multiple health-associated commensal streptococci that blocks peptide signaling and induces a common contact-dependent pattern of differential gene expression in S. mutans. Understanding the molecular basis for this inhibition will assist in the rational design of new risk assessments, diagnostics, and treatments for the most pervasive oral infectious diseases.