Zhang Jun, Chen Bo-Yan, Zhi Meng-Fan, Lin Wen-Zhen, Li Yu-Lin, Ye Hui-Lin, Xu Shuo, Zhu Hong, Zhou Lu-Jun, Du Lin-Juan, Meng Xiao-Qian, Liu Yan, Feng Qiang, Duan Sheng-Zhong
Department of Endodontics, Shanghai Ninth People's Hospital, College of Stomatology, Shanghai Jiao Tong University School of Medicine, Shanghai, Shanghai, China.
Laboratory of Oral Microbiota and Systemic Diseases, Shanghai Ninth People's Hospital, College of Stomatology, Shanghai Jiao Tong University School of Medicine; National Center for Stomatology; National Clinical Research Center for Oral Diseases; Shanghai Key Laboratory of Stomatology, Shanghai, Shanghai, China.
mSystems. 2025 Jun 17;10(6):e0008425. doi: 10.1128/msystems.00084-25. Epub 2025 May 21.
UNLABELLED: Periodontal disease (PD), an inflammatory disease initiated by oral microbiota, may aggravate hypertension (HTN). Few studies were employed to characterize the oral microbiota in hypertensive patients with periodontitis. To investigate the interplay between oral microbiota and hypertension in individuals with periodontitis, we initiated a metagenomic sequencing study on subgingival plaque and saliva samples sourced from HTN patients and those with hypertension and periodontitis (PDHTN). Our primary objective was to characterize species serving as pivotal links (bridge species) in exacerbating hypertension induced by periodontal disease. Within subgingival plaque and saliva specimens, we pinpointed 31 and 28 bridge species, respectively. Furthermore, we noted a decrease in the abundance of nitrate-reducing bacteria, such as spp., spp., and spp., in PDHTN samples. Employing network analysis, we distinguished distinct polymicrobial clusters within the two patient groups. These bridge species coalesced into polymicrobial clusters, revealing intricate symbiotic and competitive relationships. To substantiate our findings, we leveraged an angiotensin II-infused animal model of ligature-induced periodontitis (LIP), confirming the contributory role of -a selectively analyzed subgingival bridge species-in exacerbating hypertension and upregulating the frequency of renal CD4IFNγ and CD8IFNγ T cells. Our study screened a list of species linking PD and HTN. PD may aggravate HTN by decreasing the abundance of nitrate-reducing bacteria and increasing the abundance of pathogens. Using an animal model, we demonstrated that aggravates HTN via the accumulation of IFNγ T cells in the kidneys. IMPORTANCE: Both periodontal disease and hypertension are widely prevalent all over the world. PD may aggravate the development of HTN via oral microbiota. However, few studies were employed to characterize the oral microbiota in hypertensive patients with periodontitis. Here, the present study profiled the oral microbiota in hypertensive participants with periodontitis. We found that the depleted abundance of nitrate-reducing bacteria and the enriched abundance of pathogens. Finally, we validated the role of in exacerbating HTN via infiltration of IFNγ T cells in mice kidneys. Our study improved the understanding of oral microbiota linking PD and HTN.
未标记：牙周病（PD）是一种由口腔微生物群引发的炎症性疾病，可能会加重高血压（HTN）。很少有研究用于描述患有牙周炎的高血压患者的口腔微生物群特征。为了研究牙周炎患者口腔微生物群与高血压之间的相互作用，我们对来自高血压患者以及患有高血压和牙周炎（PDHTN）患者的龈下菌斑和唾液样本开展了一项宏基因组测序研究。我们的主要目标是鉴定在加重牙周病诱发的高血压过程中作为关键联系的物种（桥梁物种）。在龈下菌斑和唾液样本中，我们分别确定了31种和28种桥梁物种。此外，我们注意到在PDHTN样本中，诸如[具体菌属1]、[具体菌属2]和[具体菌属3]等硝酸盐还原菌的丰度有所下降。通过网络分析，我们在两组患者中区分出了不同的多微生物集群。这些桥梁物种聚集成多微生物集群，揭示了复杂的共生和竞争关系。为了证实我们的发现，我们利用了结扎诱导性牙周炎（LIP）的血管紧张素II灌注动物模型，证实了[一种经选择性分析的龈下桥梁物种]在加重高血压以及上调肾脏CD4IFNγ和CD8IFNγ T细胞频率方面的促成作用。我们的研究筛选出了一系列连接PD和HTN的物种清单。PD可能通过降低硝酸盐还原菌的丰度和增加病原体的丰度来加重HTN。利用动物模型，我们证明了[具体物种]通过肾脏中IFNγ T细胞的积累加重HTN。 重要性：牙周病和高血压在全球都广泛流行。PD可能通过口腔微生物群加重HTN的发展。然而，很少有研究用于描述患有牙周炎的高血压患者的口腔微生物群特征。在此，本研究描绘了患有牙周炎的高血压参与者的口腔微生物群特征。我们发现硝酸盐还原菌的丰度降低，病原体的丰度增加。最后，我们通过小鼠肾脏中IFNγ T细胞的浸润验证了[具体物种]在加重HTN中的作用。我们的研究增进了对连接PD和HTN的口腔微生物群的理解。
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