Subgingival Host-Microbial Interactions in Hyperglycemic Individuals:

摘要: Type 2 diabetes mellitus (T2DM) is an established risk factor for periodontitis, yet its contribution to creating host-bacterial disequilibrium in the subgingival crevice poorly understood. The present investigation aimed quantify impact of hyperglycemia on interactions periodontitis and map shifts these dynamics following mechanical nonsurgical therapy. Seventeen T2DM 17 non-T2DM subjects with generalized severe chronic were recruited along 20 periodontally healthy individuals. Subjects treated scaling root planing (SRP). Samples biofilm gingival crevicular fluid collected at baseline 1-, 3-, 6 mo postoperatively. Correlations generated between 13.7 million 16S ribosomal DNA sequences 8 immune mediators. Intermicrobial host-microbial modeled using differential network analysis. Periodontal health was characterized by a sparse interbacterial highly connected cytokine-bacterial network, while both normoglycemics demonstrated robust congeneric intergeneric hubs but significantly fewer connections. Following SRP, edges 2-fold increase 1 postoperatively 10-fold normoglycemics. In hyperglycemics, there doubling no further changes thereafter. These accompanied increasingly network. normoglycemics, nodes anchored interleukin (IL)-4, IL-6, IL-10 greatest rewiring, IL-1β, INF-γ, IL-17 exhibited progressive rewiring. Thus, points breakdown mutualism rather than primarily determining community assembly. Hyperglycemia exacerbates this uncoupled mutualism. Our data also demonstrate that therapy might not consistently alter microbial abundances or lower proinflammatory molecules, it "reboots" interaction immunoinflammatory system newly colonizing microbiome, restoring role bacterial colonization. However, outcome delayed hyperglycemics.