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Fusobacterium nucleatum  ( F. nucleatum ) plays key roles in the initiation and progression of periodontitis. However, the pathogenic effect of  F. nucleatum  on human oral tissues and cells has not been fully evaluated. In this study, we aimed to analyze the pathogenic effects of  F. nucleatum  on human gingival fibroblasts (GFs) and clarify the potential mechanisms. RNA-sequencing analysis confirmed that  F. nucleatum  significantly altered the gene expression of GF as the stimulation time increased. Cell counting and EdU-labeling assays indicated that  F. nucleatum  inhibited GF proliferation and promoted cell apoptosis in a time- and dose-dependent manner. In addition, cell apoptosis, intracellular reactive oxygen species (ROS) generation, and proinflammatory cytokine production were dramatically elevated after  F. nucleatum  stimulation. Furthermore, we found that the AKT/MAPK and NF- κ B signaling pathways were significantly activated by  F. nucleatum  infection and that a large number of genes related to cellular proliferation, apoptosis, ROS, and inflammatory cytokine production downstream of AKT/MAPK and NF- κ B signaling pathways were significantly altered in  F. nucleatum -stimulated GFs. These findings suggest that  F. nucleatum  inhibits GF proliferation and promotes cell apoptosis, ROS generation, and inflammatory cytokine production partly by activating the AKT/MAPK and NF- κ B signaling pathways. Our study opens a new window for understanding the pathogenic effects of periodontal pathogens on the host oral system.

oxidative medicine and cellular longevity

<i>Fusobacterium nucleatum</i>Facilitates Apoptosis, ROS Generation, and Inflammatory Cytokine Production by Activating AKT/MAPK and NF-<i>κ</i>B Signaling Pathways in Human Gingival Fibroblasts

Fusobacterium nucleatumFacilitates Apoptosis, ROS Generation, and Inflammatory Cytokine Production by Activating AKT/MAPK and NF-κB Signaling Pathways in Human Gingival Fibroblasts