Project description:Transcriptional profiling was utilized to define the biological pathways of gingival epithelial cells modulated by co-culture with the oral pathogenic Porphyromonas gingivalis and Aggregatibacter (formerly actinobacillus) actinomycetemcomitans. We used microarrays to detail the global programme of gene expression underlying infection and identified distinct classes of up- and down-regulated genes during this process. Experiment Overall Design: Gingival epithelial HIGK cells were sham infected (CTRL) and infected with either the oral pathogenic P. gingivalis (Pg) or A. actinomycetemcomitans (Aa). These samples were hybridized to Affymetrix microarrays. Understanding how host cells have adapted to pathogens, and how barrier cells respond to limit their impact, provides a mechanistic biological basis of microbial disease in the mixed bacterial-human ecosystem of the oral cavity.
Project description:Transcriptional profiling was utilized to define the biological pathways of gingival epithelial cells modulated by mono- and complex co-culture with oral commensal S. gordonii and pathogenic P. gingivalis. We used microarrays to detail the global programme of gene expression underlying infection and identified distinct classes of up- and down-regulated genes during this process. Experiment Overall Design: Gingival epithelial HIGK cells were sham infected (CTRL) and infected with either the oral commensal S. gordonii (Sg) or the pathogenic P. gingivalis (Pg) as well as co-cultured in mixed cultures of Sg and Pg (Sg+Pg). These samples were hybridized to Affymetrix microarrays. Understanding how host cells have adapted to commensals, and how barrier cells respond to limit their impact, provides a mechanistic biological basis of health in the mixed bacterial-human ecosystem of the oral cavity and provides insight on how the degree of complexity of a microbiome influences this balance.
Project description:Transcriptional profiling was utilized to define the biological pathways of gingival epithelial cells modulated by co-culture with the oral pathogenic Porphyromonas gingivalis and Aggregatibacter (formerly actinobacillus) actinomycetemcomitans. We used microarrays to detail the global programme of gene expression underlying infection and identified distinct classes of up- and down-regulated genes during this process. Keywords: infection state
Project description:Transcriptional profiling was utilized to define the biological pathways of gingival epithelial cells modulated by mono- and complex co-culture with oral commensal S. gordonii and pathogenic P. gingivalis. We used microarrays to detail the global programme of gene expression underlying infection and identified distinct classes of up- and down-regulated genes during this process. Keywords: infection state
Project description:Understanding the impact of the microbiota on oral mucosal epithelial barriers, particularly within the gingiva, is essential for elucidating the mechanisms underlying oral health and disease. The gingiva exhibits intricate tissue architecture and undergoes dynamic microenvironmental shifts influenced by various factors. Notably, microbial colonization emerges as an early-life factor that plays a significant role in shaping the functional and immunological maturation of the gingival epithelium. This study utilizes spatial transcriptomic analysis to unveil distinct immunological characteristics between the buccal and palatal regions of the murine gingiva, impacting natural alveolar bone loss. Moreover, the analysis identifies a significant influence of the microbiota on the development and function of the junctional epithelium, which faces the oral microbial plaque, offering new insights into neutrophil recruitment to this strategic location. Additionally, the microbiota is found to impact fundamental functions of the gingival epithelium, including proliferation kinetics and barrier sealing. In conclusion, this study emphasizes the crucial role played by the microbiota in regulating gingival barriers and brings attention to its unique influence on specific epithelial regions within the gingiva.
Project description:Understanding the impact of the microbiota on oral mucosal epithelial barriers, particularly within the gingiva, is essential for elucidating the mechanisms underlying oral health and disease. The gingiva exhibits intricate tissue architecture and undergoes dynamic microenvironmental shifts influenced by various factors. Notably, microbial colonization emerges as an early-life factor that plays a significant role in shaping the functional and immunological maturation of the gingival epithelium. This study utilizes spatial transcriptomic analysis to unveil distinct immunological characteristics between the buccal and palatal regions of the murine gingiva, impacting natural alveolar bone loss. Moreover, the analysis identifies a significant influence of the microbiota on the development and function of the junctional epithelium, which faces the oral microbial plaque, offering new insights into neutrophil recruitment to this strategic location. Additionally, the microbiota is found to impact fundamental functions of the gingival epithelium, including proliferation kinetics and barrier sealing. In conclusion, this study emphasizes the crucial role played by the microbiota in regulating gingival barriers and brings attention to its unique influence on specific epithelial regions within the gingiva.
Project description:Understanding the impact of the microbiota on oral mucosal epithelial barriers, particularly within the gingiva, is essential for elucidating the mechanisms underlying oral health and disease. The gingiva exhibits intricate tissue architecture and undergoes dynamic microenvironmental shifts influenced by various factors. Notably, microbial colonization emerges as an early-life factor that plays a significant role in shaping the functional and immunological maturation of the gingival epithelium. This study utilizes spatial transcriptomic analysis to unveil distinct immunological characteristics between the buccal and palatal regions of the murine gingiva, impacting natural alveolar bone loss. Moreover, the analysis identifies a significant influence of the microbiota on the development and function of the junctional epithelium, which faces the oral microbial plaque, offering new insights into neutrophil recruitment to this strategic location. Additionally, the microbiota is found to impact fundamental functions of the gingival epithelium, including proliferation kinetics and barrier sealing. In conclusion, this study emphasizes the crucial role played by the microbiota in regulating gingival barriers and brings attention to its unique influence on specific epithelial regions within the gingiva.
Project description:Emerging evidence indicates that gingival-resident helper CD4+ T cells are major drivers of periodontal inflammation in response to commensal and pathogenic oral microorganisms. Whether tissue-resident memory CD8+ T cells (TRM), which principally safeguard against viruses and cancer but also drive certain autoimmune and inflammatory conditions, impact periodontitis progression and severity remain unknown. We asked whether local reactivation of oral CD8+ TRM of a defined antigen specificity could exacerbate ligature-induced periodontitis (LIP), a well-established model of periodontal disease in mice. Topical application of virus-mimicking peptides to the oral mucosa concurrent with LIP 1) intensified alveolar bone loss, 2) amplified gingival and cervical lymph node inflammation, and 3) stimulated gingival transcriptional changes in genes related to innate immune sensing and cell-mediated cytotoxicity. Therapeutic depletion of CD103-expressing oral CD8+ TRM in advance of LIP prevented exacerbation of disease. These observations provide evidence that oral CD103+ CD8+ TRM have the potential to participate in gingival inflammation, alveolar bone loss, and periodontitis.