| Periodontal diseases result from bacterial infection by several pathogens combined with a destructive host immune response. Host-pathogen interactions are inherently dynamic and complex and the unique environment of the oral cavity further complicates the relationship between hosts and microbes. It is estimated that more than 700 bacterial species can inhabit the oral cavity, and a single individual may support 30 to 80 bacterial species at a given time. These bacteria interact with each other as well as with the host, and the impact of additional factors such as smoking or diabetes mellitus further influences the state of health or disease. Although there are many risk factors associated with periodontal disease, true prognostic indicators are lacking and require development. To achieve this goal, gaining an understanding of the host pathogen interactions in the oral cavity, and determining key events that shift the balance from health to illness are crucial aspects of effectively treating periodontal disease.;This study utilized transcriptional profiling to investigate the interactions between human immortalized gingival keratinocytes (HIGKs) and two oral pathogens, Aggregatibacter actinomycetemcomitans and Porphyromonas gingivalis . A model using HIGK cells was developed, and the most-impacted host pathways were further characterized phenotypically. Insights gained were related to tropism of oral bacteria to oral epithelia, a specific epithelial response to different species of bacteria, and the contribution of specific bacterial components to the bacterial-host interactions. The impacts of P. gingivalis YPF1, A. actinomycetemcomitans CDT, ORF859, and Aae upon the host transcriptome were investigated. In collaboration with other researchers, the impact of P. gingivalis SerB was also studied. Also in collaboration, the interactions of epithelial cells to commensal S. gordonii and the opportunistic commensal F. nucleatum have been initiated.;This work focuses on the host-pathogen interplay occurring in the oral epithelium. The model system established, and the insights provided herein based on host cell global responses will lead to a greater understanding of host pathogen interactions. |
