ArticlePloS one2017
Transcriptome profiling analysis of senescent gingival fibroblasts in response to Fusobacterium nucleatum infection.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 37 citations in OpenAlex.
- Quantitative assessment of specific bacterial taxa of the intestinal microbiota of healthy and diarrheic horses.Journal of veterinary internal medicine · 2026Article
- Fusobacterium nucleatum promotes senescence of human oral mucosa fibroblasts via the Wnt5A/mTOR pathway.Odontology · 2026Article
- Mucosa-associated bacteria and metabolites in inflammatory bowel disease: from inside to insight.NPJ biofilms and microbiomes · 2026Review
- Article
- Review
- Cross-omics analysis reveals microbe-metabolism interactions characteristic of gingival enlargement associated with fixed orthodontic in adolescents.Journal of oral microbiology · 2025Article
- IntratumoralPathogens (Basel, Switzerland) · 2024Review
- Molecular Signatures of Senescence in Periodontitis: Clinical Insights.Journal of dental research · 2024Article
- Fusobacterium nucleatum infection modulates the transcriptome and epigenome of HCT116 colorectal cancer cells in an oxygen-dependent manner.Communications biology · 2024Article
- Fusobacterium nucleatum triggers senescence phenotype in gingival epithelial cells.Molecular oral microbiology · 2024Article
- A bibliometric and visualized in oral microbiota and cancer research from 2013 to 2022.Discover oncology · 2024Article
- The Role ofMicroorganisms · 2023Review
- Pathogenesis of periodontitis - A potential role for epithelial-mesenchymal transition.The Japanese dental science review · 2022Review
- Periodontal connection with intestinal inflammation: Microbiological and immunological mechanisms.Periodontology 2000 · 2022Review
- Review
- Creutzfeldt-Jakob Disease: Alterations of Gut Microbiota.Frontiers in neurology · 2022Article
- Oral microbiota in the oral-genitourinary axis: identifying periodontitis as a potential risk of genitourinary cancers.Military Medical Research · 2021Review
- Effect of Aging on Homeostasis in the Soft Tissue of the Periodontium: A Narrative Review.Journal of personalized medicine · 2021Review
- Role of the oral microbiota in cancer evolution and progression.Cancer medicine · 2020Review
- Characterization of the Esophageal Microbiota and Prediction of the Metabolic Pathways Involved in Esophageal Cancer.Frontiers in cellular and infection microbiology · 2020Article
Corrections and comments
- Erratum issued
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Periodontal disease is caused by dental plaque biofilms. Fusobacterium nucleatum is an important periodontal pathogen involved in the development of bacterial complexity in dental plaque biofilms. Human gingival fibroblasts (GFs) act as the first line of defense against oral microorganisms and locally orchestrate immune responses by triggering the production of reactive oxygen species and pro-inflammatory cytokines (IL-6 and IL-8). The frequency and severity of periodontal diseases is known to increase in elderly subjects. However, despite several studies exploring the effects of aging in periodontal disease, the underlying mechanisms through which aging affects the interaction between F. nucleatum and human GFs remain unclear. To identify genes affected by infection, aging, or both, we performed an RNA-Seq analysis using GFs isolated from a single healthy donor that were passaged for a short period of time (P4) 'young GFs' or for longer period of time (P22) 'old GFs', and infected or not with F. nucleatum. Comparing F. nucleatum-infected and uninfected GF(P4) cells the differentially expressed genes (DEGs) were involved in host defense mechanisms (i.e., immune responses and defense responses), whereas comparing F. nucleatum-infected and uninfected GF(P22) cells the DEGs were involved in cell maintenance (i.e., TGF-β signaling, skeletal development). Most DEGs in F. nucleatum-infected GF(P22) cells were downregulated (85%) and were significantly associated with host defense responses such as inflammatory responses, when compared to the DEGs in F. nucleatum-infected GF(P4) cells. Five genes (GADD45b, KLF10, CSRNP1, ID1, and TM4SF1) were upregulated in response to F. nucleatum infection; however, this effect was only seen in GF(P22) cells. The genes identified here appear to interact with each other in a network associated with free radical scavenging, cell cycle, and cancer; therefore, they could be potential candidates involved in the aged GF's response to F. nucleatum infection. Further studies are needed to confirm these observations.
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