Capacity of Oral Commensal Bacteria to Control Epithelial Cell Inflammation

Objectives: Periodontal disease can manifest when there is an imbalance within the host oral bacteria resulting in chronic inflammation and ultimately leading soft tissue damage and bone loss. Suppression of the inflammatory response may lead to slowing periodontal disease. The objective of this study was to determine a mechanism for commensal bacteria to control epithelial inflammation.
Methods: Human oral epithelial cell line, OKF4s were grown to sub-confluent or confluent culture and challenged with either Streptococcus gordonii or Porphyromonas gingivalis. Gene expression profiles for NRF-2, IRAK-3, CD-180, FCAR, and IL-32 were analyzed via qPCR. IL-8 expression was evaluated as a biomarker of inflammatory response.
Results: No change in expression of IRAK-3 in either confluent or sub-confluent cells was observed. NRF-2 showed slight increase in gene expression in confluent and subconfluent cells. After bacterial insult, relative gene expression increased in both CD-180 subconfluent cells and IL-8 confluent cells. Contrastingly, relative gene expression was decreases within CD-180 confluent and FCAR subconfluent cells. Overall gene expression between confluent and subconfluent cells were as follows: IL-32 and IL-8 cells showed a marked increase in gene expression while CD-180 and FCAR subconfluent cells decreased in gene expression when compared to their confluent cell counterparts.
Conclusions: While NRF-2 shows only slight changes in expression, these differences can have vast downstream effects. Other genes show a much larger change in gene expression which could indicate that our bacterial challenge is inducing an inflammatory response in which these genes play a crucial role. Furthermore, the extreme differences in gene expression between subconfluent and confluent cells could suggest that tissue may act differently in a healthy state versus a wound healing state.