Potassium is a key signal in host-microbiome dysbiosis in periodontitis.
Potassium is a key signal in host-microbiome dysbiosis in periodontitis.
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DOI：
10.1371/journal.ppat.1006457
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发表时间：
2017-06
期刊：
影响因子：
6.7
通讯作者：
Frias-Lopez J
中科院分区：
文献类型：
--
作者：
Yost S;Duran-Pinedo AE;Krishnan K;Frias-Lopez J
微生物群的结构和/或功能特性的失衡是炎症性肠病(IBD)和牙周病等重要感染性炎症性疾病的根源。牙周炎是一种多菌炎性疾病，影响着世界上很大一部分人口，并与各种全身健康状况有关，如糖尿病、心血管疾病和呼吸系统疾病。生物失调已被认为是该病发展的一个关键因素。然而，导致人类微生物组失调的确切机制和环境信号在很大程度上是未知的。在先前的一系列活体研究中，通过对牙周炎及其进展的后转录分析，我们确定了几个与疾病高度相关的功能特征。其中，钾离子转运似乎是发病过程中的关键。为了证实其重要性，我们进行了一系列的体外实验，在这些实验中，我们证明了钾水平增加了整个口腔群落的毒力，同时改变了牙龈上皮的免疫反应，增加了肿瘤坏死因子-α的产生，减少了IL-6和抗菌肽hBD-3(hBD-3)的表达。这些结果表明，牙周袋中的钾水平可能是口腔微生物群失调的一个重要因素。它们是识别关键环境信号的起点，这些信号将口腔微生物群落的行为从共生群落改变为非共生群落。人体微生物群的动态平衡对维持人体的健康状态起着关键作用。人类微生物组组成和功能的变化(生物失调)是炎症性肠病(IBD)和牙周病等重要感染性炎症性疾病的根源。然而，引发非生态型疾病发展的环境因素在很大程度上是未知的。在以前的研究中，我们利用全社会范围的转录组分析，发现离子钾转运在牙周炎的发病机制及其进展中是最重要的功能之一。在这里，我们通过一系列的体外实验证实，钾可以作为一个重要的信号，在口腔微生物组中诱导致病机理，并在微生物挑战面前改变宿主反应，从而可能导致微生物免疫颠覆。我们的研究为离子钾在牙周炎期间口腔生物失调中的重要作用提供了新的见解。
Dysbiosis, or the imbalance in the structural and/or functional properties of the microbiome, is at the origin of important infectious inflammatory diseases such as inflammatory bowel disease (IBD) and periodontal disease. Periodontitis is a polymicrobial inflammatory disease that affects a large proportion of the world's population and has been associated with a wide variety of systemic health conditions, such as diabetes, cardiovascular and respiratory diseases. Dysbiosis has been identified as a key element in the development of the disease. However, the precise mechanisms and environmental signals that lead to the initiation of dysbiosis in the human microbiome are largely unknown. In a series of previous in vivo studies using metatranscriptomic analysis of periodontitis and its progression we identified several functional signatures that were highly associated with the disease. Among them, potassium ion transport appeared to be key in the process of pathogenesis. To confirm its importance we performed a series of in vitro experiments, in which we demonstrated that potassium levels a increased the virulence of the oral community as a whole and at the same time altering the immune response of gingival epithelium, increasing the production of TNF-α and reducing the expression of IL-6 and the antimicrobial peptide human β-defensin 3 (hBD-3). These results indicate that levels of potassium in the periodontal pocket could be an important element in of dysbiosis in the oral microbiome. They are a starting point for the identification of key environmental signals that modify the behavior of the oral microbiome from a symbiotic community to a dysbiotic one. Homeostasis of the human microbiome plays a key role in maintaining the healthy status of the human body. Changes in composition and function of the human microbiome (dysbiosis) are at the origin of important infectious inflammatory diseases such as inflammatory bowel disease (IBD) and periodontal disease. However, the environmental elements that trigger the development of dysbiotic diseases are largely unknown. In previous studies, using community-wide transcriptome analysis, we identified ion potassium transport as one of the most important functions in the pathogenesis of periodontitis and its progression. Here, we confirm with a series of in vitro experiments that potassium can act as an important signal in the dysbiotic process inducing pathogenesis in the oral microbiome and altering the host response in front of the microbial challenge that could lead to microbial immune subversion. Our study provides new insights into the important role that ion potassium plays a signal in oral dysbiosis during periodontitis.