The Forsyth Institute, Cambridge, MA 02142, USA.
Division of Geological and Planetary Sciences, California Institute of Technology, Pasadena, CA 91125, USA.
Cell Host Microbe. 2021 Nov 10;29(11):1649-1662.e7. doi: 10.1016/j.chom.2021.09.009. Epub 2021 Oct 11.
Saccharibacteria (TM7) are obligate epibionts living on the surface of their host bacteria and are strongly correlated with dysbiotic microbiomes during periodontitis and other inflammatory diseases, suggesting they are putative pathogens. However, due to the recalcitrance of TM7 cultivation, causal research to investigate their role in inflammatory diseases is lacking. Here, we isolated multiple TM7 species on their host bacteria from periodontitis patients. These TM7 species reduce inflammation and consequential bone loss by modulating host bacterial pathogenicity in a mouse ligature-induced periodontitis model. Two host bacterial functions involved in collagen binding and utilization of eukaryotic sialic acid are required for inducing bone loss and are altered by TM7 association. This TM7-mediated downregulation of host bacterial pathogenicity is shown for multiple TM7/host bacteria pairs, suggesting that, in contrast to their suspected pathogenic role, TM7 could protect mammalian hosts from inflammatory damage induced by their host bacteria.
厚壁菌门（TM7）是严格的专性表面共生菌，生活在宿主细菌的表面，与牙周炎和其他炎症性疾病中的失调微生物组强烈相关，这表明它们是潜在的病原体。然而，由于 TM7 的培养具有顽固性，因此缺乏关于它们在炎症性疾病中的作用的因果关系研究。在这里，我们从牙周炎患者的宿主细菌上分离出多种 TM7 物种。这些 TM7 物种通过调节宿主细菌的致病性，在小鼠结扎诱导的牙周炎模型中减轻炎症和随之发生的骨质流失。两种与胶原结合和利用真核唾液酸有关的宿主细菌功能是导致骨质流失所必需的，并且会被 TM7 的关联所改变。这种 TM7 介导的宿主细菌致病性下调在多种 TM7/宿主细菌对中都有体现，这表明与它们疑似的致病性作用相反，TM7 可以保护哺乳动物宿主免受其宿主细菌引起的炎症性损伤。
