Abstract
Objective: This study focused on documenting characteristics of the gingival transcriptome during various stages of periodontitis targeting genes associated with apoptotic and autophagic pathways and changes that specifically associate with features of the oral microbiome.Methods: Macaca mulatta (n = 18; 12–23 years) were examined at baseline and 0.5, 1, and 3 months of disease progression, as well as 5 months with clinical disease resolution. 16S sequencing and microarray analyses examined changes in the microbiome and gingival transcriptome, respectively, at each time point from every animal.Results: Specific patterns of apoptotic and autophagic genes were identified related to the initiation and progression of disease. The analysis also provided insights on the principal bacteria within the complex microbiome whose abundance was significantly correlated with differences in apoptotic and autophagic gene expression. Bacteria were identified that formed associated complexes with similar effects on the host gene expression profiles. A complex of Leptotrichia_unclassifed, Capnocytophaga_unclassified, Prevotella sp. 317, and Veillonellaceae_[G-1] sp. 155 were significantly negatively correlated with both apoptosis and autophagy. Whereas, Veillonellaceae_[G-1], Porphyromonadaceae, and F. alocis 539 were significantly positively correlated with both pathways, albeit this relationship was primarily associated with pro-apoptotic genes.Conclusions: The findings provide evidence for specific bacteria/bacterial complexes within the oral microbiome that appear to have a more substantive effect on regulating apoptotic and autophagic pathways in the gingival tissues with periodontitis.
Highlights
Mucosal surfaces of the body, including the oral cavity, are continually interacting with a complex microbiome [1]
Chronic periodontitis reflects an active breakdown of connective tissue and resorption of alveolar bone, with localized lesions attributed to a dysregulated host inflammatory and immune responses to dysbiotic microbial biofilms [7,8,9,10,11,12]
Microbiome changes with disease have been shown to include alterations in specific members of the subgingival microbiome at disease sites (e.g., Porphyromonas gingivalis) with the capacity to alter the biologic activities of the overall microbiome, as well as regulating host responses that would contribute to the tissue breakdown as a hallmark of periodontitis [13, 14]
Summary
Mucosal surfaces of the body, including the oral cavity, are continually interacting with a complex microbiome [1]. This challenge results in activation of an array of immune response pathways, and cells and biomolecules that maintain homeostasis. The oral cavity presents a model of mucosal hostbacterial interactions whereby specific microorganisms colonize various niches [2] creating complex biofilms that change with local environmental cues and respond to disease processes of the periodontium [3,4,5,6]. Various microbial species appear to modulate autophagy as a virulence strategy to enable persistent survival inside host cells affecting both anti-microbial and anti-inflammatory responses [24, 25]
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