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Comparison of Genetic and Epigenetic Profiles of Periodontitis According to the Presence of Type 2 Diabetes

ABSTRACT: Type 2 diabetes mellitus (T2DM) and periodontitis (PD) have intricate connections as chronic inflammatory diseases. While the immune response is a key factor that accounts for their association, the underlying mechanisms remain unclear. To gain a deeper understanding of the connection, we conducted research using a multi-omics approach. We generated whole genome and EPIC array data from the periodontium of PD patients with DM (PDDM) and without DM to confirm genetic and epigenetic changes. Independent bulk and single-cell RNA sequencing data were employed to verify the expression levels of hypo-methylated genes. We observed a gradual rise in C>T base substitutions and hypomethylation in PD and PDDM patients compared to healthy participants. Furthermore, specific genetic and epigenetic alterations were prominently associated with the Fc gamma receptor-mediated phagocytosis pathway. The upregulation of these genes was confirmed in both the periodontal tissues of PD patients and the pancreatic tissues of T2DM patients. Through single-cell RNA analysis of peripheral blood mononuclear cells, substantial upregulation of Fc gamma receptors and related genes was particularly identified in monocytes. Our findings suggest that targeting the Fc-gamma signaling pathway in monocytes holds promise as a potential treatment strategy for managing systemic complications associated with diabetes.

ORGANISM(S): Homo sapiens

PROVIDER: GSE267170 | GEO | 2024/06/28

REPOSITORIES: GEO

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Project description:BACKGROUND: Pulmonary tuberculosis (PTB) and diabetes mellitus (DM) are prevalent chronic diseases with substantial implications for human health. DM patients are more susceptible to PTB, which exacerbates diabetes-related complications. However, the complex molecular mechanisms underlying the enhanced susceptibility of DM patients to PTB infection remain poorly understood. RESULTS: α-and β-diversity of gut microbiota were significantly reduced in PTB patients and PTB-DM patients. In addition, the abundances of families Lachnospiraceae and Ruminococcaceae in Firmicutes phylum were downregulated in PTB patients and further diminished in PTB-DM patients. On the other hand, untargeted metabolomics in frozen serum and stool samples indicated that such as Phenylalanine, tyrosine and tryptophan biosynthesis, Arginine and proline metabolism, Tryptophan metabolism and Histidine metabolism et al were consistently and significantly altered in PTB patients and PTB-DM patients, with the significant upregulation of most metabolites. Amino acids like serine, proline, histidine et al were both remarkably elevated in PTB and PTB-DM patients. The correlation network analysis reveals the relationships between the shared microbial biomarkers and the shared metabolic pathways. CONCLUSIONS: This research contributes to the exploration of pivotal diagnostic biomarkers for both patients with PTB and PTB accompanied by diabetes. Specifically, shared reductions were identified in the genera g-Roseburia, g-Ruminococcaceae_UCG.013, g-Ruminococcaceae_NK4A214, g-Lachnospiraceae_unclassified and g-Firmicutes_unclassified, in addition to notable regulation of amino acids like glycine, serine and histine in patients with PTB and PTB-DM. Our study expands the comprehension of the intricate connections linking gut microbiota, fecal metabolites and serum metabolites in PTB and PTB-DM patients.

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Comparison of Genetic and Epigenetic Profiles of Periodontitis According to the Presence of Type 2 Diabetes

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