Project description:Porphyromonas gingivalis and Treponema denticola are periodontalpathogens that are associated with the severity and progression of periodontal diseases. This study investigates the gene expression of Porphyromonas gingivalis during co-culture with Treponema denticola
Project description:Porphyromonas gingivalis and Treponema denticola are periodontalpathogens that are associated with the severity and progression of periodontal diseases. this study investigates the gene expression of Treponema denticola during co-culture with Porphyromonas gingivalis.
Project description:Wild type Porphyromonas gingivalis strain ATCC33277 (V3176) and PG1626 - deficient mutant (V3177) were grown in iron replete conditions was used to compare to Porphyromonas gingivalis strains grown in iron chelated conditions.
Project description:Recent epidemiological studies revealed a significant association between oral squamous cell carcinoma (OSCC) and Porphyromonas gingivalis, a major pathogen of periodontal disease. As a keystone pathogen, P. gingivalis is known not only to damage local periodontal tissue, but also to evade from the host immune system and eventually affect systemic health. However, its role in OSCC has yet to be well studied. To explore the underlying effect of chronic P. gingivalis infection on OSCC and to identify relevant biomarkers as promising targets for therapy and prevention, we established a novel model by exposing human immortalized oral epithelial cells (HIOECs) to P. gingivalis at a low MOI for 5 to 23 weeks. The P. gingivalis-infected HIOECs were monitored in tumor biological alteration. Bioinformatics analyses were performed on HIOECs infected for 15 weeks, and some selected data were validated by q-PCR and (or) Western blot on cells infected for 15 and 23 weeks. Accordingly, we found that persistent exposure to P. gingivalis induced tumor biological properties on HIOECs. Tumor-related genes such as NNMT, FLI1, GAS6, lncRNA CCAT1, PDCD1LG2 and CD274 were aberrantly expressed in response to long-term exposure of P. gingivalis. In addition, some clinical biomarkers and novel proteins were presented. In conclusion, chronic P. gingivalis infection may be a potential risk factor of OSCC. The key regulators and biomarkers might be used in monitoring OSCC with chronic periodontal infection. We applied lncRNA Microarray (Affymetrix) which could simultaneously detect coding and non-coding genes to explore the differences of cell gene expression after long-term exposure to P. gingivalis.
Project description:We use high through put RNA sequenceing technology to study the genome-wide expression profile in an oral pathogen Filifactor alocis when co-cultured with another key-stone oral pathogen Porphyromonas gingivalis under anaerobic conditions and oxidative stress conditions.
Project description:Genotyping studies suggest that there is genetic variability among P. gingivalis strains, however the extent of variability remains unclear, and the regions of variability have only partially been identified. We previously used heteroduplex analysis of the ribosomal operon intergenic spacer region (ISR) to type P. gingivalis strains in several diverse populations, identifying 6 predominant heteroduplex types and many minor ones. In addition we used ISR sequence analysis to determine the relatedness of P. gingivalis strains to one another, and demonstrated a link between ISR sequence phylogeny and the disease-associated phenotype of P. gingivalis strains. The availability of whole genome microarrays based on the genomic sequence of strain W83 has allowed a more comprehensive analysis of P. gingivalis strain variability, using the entire genome. The objectives of this study were to define the phylogeny of P. gingivalis strains using the entire genome, to compare the phylogeny based on genome content to the phylogeny based on a single locus (ISR), and to identify genes that are associated with the strongly disease-associated strain W83 that could be important for virulence. Keywords: Comparative genomic hybridization
Project description:To determine the biological mechanisms underlying a dampened immune response to Porphyromonas gingivalis, as compared to Aggregatibacter actinomycetemcomitans challenge, we infected primary BMDCs with either pathogen or left uninfected Total RNA from uninfected BMDCs compared to BMDCs infected with either Aggregatibacter actinomycetemcomitans or Porphyromonas gingivalis
Project description:Periodontitis and infections with periodontal bacteria have been highlighted as risk factors for dementia. In recent years attention has been drawn to the role of microglia cells in neurodegenerative diseases. However, there is limited knowledge of the influence of periodontal bacteria on microglia cells. The aim of the present study was to investigate the interactions between the periodontal bacteria P. gingivalis and microglia cells, and to unravel if these interactions could contribute to Alzheimer’s pathology. Periodontitis and infections with periodontal bacteria have been highlighted as risk factors for dementia. In recent years attention has been drawn to the role of microglia cells in neurodegenerative diseases. However, there is limited knowledge of the influence of periodontal bacteria on microglia cells. The aim of the present study was to investigate the interactions between the periodontal bacteria P. gingivalis and microglia cells, and to unravel if these interactions could contribute to Alzheimer’s pathology. We found, through microarray analysis, that stimulation of microglia cells with P. gingivalis resulted in upregulation of several Alzheimer´s disease associated genes, including NOX4. We also showed that P. gingivalis LPS mediated ROS production and IL-6 and IL-8 induction via NOX4 in microglia. The viability of neurons was shown to be reduced by conditioned media from microglia cells stimulated with P. gingivalis LPS, and that the reduction was NOX4 dependent. The levels of total and phosphorylated Tau in neurons were increased by conditioned media from microglia cells stimulated with P. gingivalis or LPS. This increase was NOX4 dependent. In summary our findings give us a potential mechanistic explanation of how the periodontal pathogen P. gingivalis could trigger or exacerbate AD pathogenesis.