ArticleFrontiers in cell and developmental biology2026
Investigating the causal impact of gut microbiota on periodontitis based on Mendelian randomization, bulk transcriptomics, and single-cell transcriptomics.
Article in Frontiers in cell and developmental biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Dysbiosis of the gut microbiota is closely associated with periodontitis (PD), yet whether a direct causal relationship exists and the underlying molecular mechanisms remain unclear. This study aims to identify key genes linking gut microbiota to PD, providing molecular targets for its precise prevention, diagnosis, and treatment. Methods: Three PD-related transcriptomic datasets (GSE10334, GSE223924, GSE171213) were obtained from public databases. Through Mendelian randomization (MR), machine learning, and expression validation, key regulatory genes causally linking gut microbiota to PD were identified. Gingival tissue specimens from PD patients (n = 6) and healthy controls (n = 6) were used for independent validation via quantitative real-time PCR(qRT-PCR) and Western blot. Immune cell infiltration analysis and cell communication network analysis were further conducted using single-cell RNA sequencing data. Results: MR analysis identified 22 gut microbiota taxa causally associated with PD (12 protective, OR<1; 10 risk-associated, OR>1). Transcriptomic analysis yielded seven candidate genes, which were narrowed to 4 feature genes via multi-algorithm machine learning. Cross-dataset validation confirmed three key genes-IL-19, NID2, and SH3D19-with consistent differential expression. Independent experimental validation confirmed significant upregulation of NID2 at both mRNA and protein levels in the PD group ( Conclusion: This multi-omics study identified 22 gut microbiota taxa causally associated with PD, and IL-19, NID2, and SH3D19 as key dysregulated genes. Among these, NID2 emerged as a prioritized candidate linking gut dysbiosis to periodontitis, warranting further functional investigation. These findings provide molecular evidence for the oral-gut axis and offer potential biomarkers and therapeutic targets for PD.
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