Selenomonas sputigena Interactions with Gingival Epithelial Cells That Promote Inflammation

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 approac...

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Bibliographic Details
Published in:Infection and immunity 2023-02, Vol.91 (2), p.e0031922-e0031922
Main Authors: Hawkes, Colin G, Hinson, Annie N, Vashishta, Aruna, Read, Curtis B, Carlyon, Jason A, Lamont, Richard J, Uriarte, Silvia M, Miller, Daniel P
Format: Article
Language:English
Subjects:
Cellular Microbiology: Pathogen-Host Cell Molecular Interactions
Cytokines - metabolism
Epithelial Cells - metabolism
Host-Microbial Interactions
Humans
Inflammation
Periodontal Diseases
Periodontitis - pathology
Porphyromonas gingivalis - metabolism
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Summary: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.
ISSN:0019-9567
1098-5522
DOI:10.1128/iai.00319-22