Philips Institute for Oral Health Research, Virginia Commonwealth University School of Dentistry, Richmond, Virginia, USA.
Department of Microbiology and Immunology, Virginia Commonwealth University School of Medicine, Richmond, Virginia, USA.
Infect Immun. 2023 Feb 16;91(2):e0031922. doi: 10.1128/iai.00319-22. Epub 2023 Jan 17.
Increased prevalence and abundance of Selenomonas sputigena have been associated with periodontitis, a chronic inflammatory disease of tooth-supporting tissues, for more than 50 years. Over the past decade, molecular surveys of periodontal disease using 16S and shotgun metagenomic sequencing approaches have confirmed the disease association of classically recognized periodontal pathogens such as Porphyromonas gingivalis, Treponema denticola, and Tannerella forsythia while highlighting previously underappreciated organisms such as Filifactor alocis and S. sputigena. Despite abundant clinical association between and periodontal disease, we have little to no understanding of its pathogenic potential, and virulence mechanisms have not been studied. In this study, we sought to characterize the response of gingival epithelial cells to infection with . Here, we show that attaches to gingival keratinocytes and induces expression and secretion of cytokines and chemokines associated with inflammation and leukocyte recruitment. We demonstrate that induces signaling through Toll-like receptor 2 (TLR2) and TLR4 but evades activation of TLR5. Cytokines released from -infected keratinocytes induced monocyte and neutrophil chemotaxis. These results show that S. -host interactions have the potential to contribute to bacterially driven inflammation and tissue destruction, the hallmark of periodontitis. Characterization of previously unstudied pathogens may provide novel approaches to develop therapeutics to treat or prevent periodontal disease.
超过 50 年来,栖牙密螺旋体(Selenomonas sputigena)的患病率和丰度增加与牙周炎有关,牙周炎是一种牙齿支持组织的慢性炎症性疾病。在过去的十年中,使用 16S 和 shotgun 宏基因组测序方法对牙周病进行的分子调查证实了经典的牙周病原体如牙龈卟啉单胞菌(Porphyromonas gingivalis)、齿密螺旋体(Treponema denticola)和福赛斯坦纳菌(Tannerella forsythia)与疾病的关联,同时也强调了以前被低估的生物体,如纤黏蛋白菌(Filifactor alocis)和栖牙密螺旋体。尽管 与牙周病之间存在丰富的临床关联,但我们对其致病潜力几乎一无所知,也没有研究其毒力机制。在这项研究中,我们试图描述牙龈上皮细胞对 感染的反应。在这里,我们表明 附着在牙龈角蛋白细胞上,并诱导与炎症和白细胞募集相关的细胞因子和趋化因子的表达和分泌。我们证明 通过 Toll 样受体 2(TLR2)和 TLR4 诱导信号转导,但逃避 TLR5 的激活。来自 感染角蛋白细胞释放的细胞因子诱导单核细胞和中性粒细胞趋化。这些结果表明,S. -宿主相互作用有可能导致细菌驱动的炎症和组织破坏,这是牙周炎的标志。对以前未研究的病原体的特征分析可能为开发治疗牙周病的治疗方法或预防方法提供新的途径。