PDF(Pubmed)
Abstract：
Oral bacteria are implicated not only in oral diseases but also in gut dysbiosis and inflammatory conditions throughout the body. The periodontal pathogen Aggregatibacter actinomycetemcomitans (Aa) often occurs in complex oral biofilms with Streptococcus gordonii (Sg), and this interaction might influence the pathogenic potential of this pathogen. This study aims to assess the impact of oral inoculation with Aa, Sg, and their association (Aa+Sg) on alveolar bone loss, oral microbiome, and their potential effects on intestinal health in a murine model. Sg and/or Aa were orally administered to C57Bl/6 mice, three times per week, for 4 weeks. Aa was also injected into the gingiva three times during the initial experimental week. After 30 days, alveolar bone loss, expression of genes related to inflammation and mucosal permeability in the intestine, serum LPS levels, and the composition of oral and intestinal microbiomes were determined. Alveolar bone resorption was detected in Aa, Sg, and Aa+Sg groups, although Aa bone levels did not differ from that of the SHAM-inoculated group. Il-1β expression was upregulated in the Aa group relative to the other infected groups, while Il-6 expression was downregulated in infected groups. Aa or Sg downregulated the expression of tight junction genes Cldn 1, Cldn 2, Ocdn, and Zo-1 whereas infection with Aa+Sg led to their upregulation, except for Cldn 1. Aa was detected in the oral biofilm of the Aa+Sg group but not in the gut. Infections altered oral and gut microbiomes. The oral biofilm of the Aa group showed increased abundance of Gammaproteobacteria, Enterobacterales, and Alloprevotella, while Sg administration enhanced the abundance of Alloprevotella and Rothia. The gut microbiome of infected groups showed reduced abundance of Erysipelotrichaceae. Infection with Aa or Sg disrupts both oral and gut microbiomes, impacting oral and gut homeostasis. While the combination of Aa with Sg promotes Aa survival in the oral cavity, it mitigates the adverse effects of Aa in the gut, suggesting a beneficial role of Sg associations in gut health.
摘要：
口腔细菌不仅与口腔疾病有关，而且与整个身体的肠道菌群失调和炎症有关。牙周病原体放线菌Aggregatibacter放线菌（Aa）通常发生在具有格氏链球菌（Sg）的复杂口腔生物膜中，这种相互作用可能会影响这种病原体的致病潜力。本研究旨在评估口服接种Aa的影响，Sg,以及它们与牙槽骨丢失的关联(Aa+Sg)，口腔微生物组，以及它们对小鼠模型肠道健康的潜在影响。将Sg和/或Aa口服给予C57Bl/6小鼠,每周三次,4周。在最初的实验周期间，Aa也被注射到牙龈中三次。30天后,牙槽骨丢失,肠道炎症和粘膜通透性相关基因的表达，血清LPS水平，并测定了口腔和肠道微生物的组成。在Aa中检测到牙槽骨吸收，Sg,Aa+Sg组,尽管Aa骨水平与SHAM接种组没有差异。IL-1β表达在Aa组中相对于其他感染组上调,而IL-6表达在感染组中下调。Aa或Sg下调紧密连接基因Cldn1，Cldn2，Ocdn，和Zo-1，而Aa+Sg感染导致它们的上调，除了Cldn1。在Aa+Sg组的口腔生物膜中检测到Aa，但在肠道中未检测到。感染改变了口腔和肠道微生物组。Aa组的口腔生物膜显示出增加的γ蛋白细菌丰度，肠杆菌,和Alloprevotella,而Sg管理增强了Alloprevotella和Rothia的丰度。感染组的肠道微生物组显示出丹毒科的丰度降低。Aa或Sg感染会破坏口腔和肠道微生物组，影响口腔和肠道稳态。虽然Aa与Sg的组合可促进Aa在口腔中的存活，它减轻了Aa在肠道中的不利影响，提示Sg关联在肠道健康中的有益作用。
