Expression of ssrA in non-pathogen-induced adaptation in the oral cavity through signal exchange with oral pathogens

Introduction: This study was conducted to evaluate ssrA expression resulting from adaptation of Escherichia coli (E. coli) to oral pathogens through signal exchange. Materials and Methods: Human cell lines Hep2 and HT29, wild-type E. coli (WT K-12), ssrA knock-out E. coli (${\Delta}K$-12), and Scleropages aureus (S. aureus) were used. A single culture consisting of Hep2, HT29, WT K-12, and ${\Delta}K$-12, and mixed cultures consisting of Hep2 and WT K-12, Hep2 and ${\Delta}K$-12, WT K-12 and S. aureus, ${\Delta}K$-12 and S. aureus, and Hep2, WT K-12, and S. aureus were prepared. For HT29, a mixed culture was prepared with WT K-12 and with WT K-12 and S. aureus. Total RNA was extracted from each culture with the resulting expression of ssrA, nuclear factor kappa-light-chain-enhancer of activated B cells (NF-${\kappa}B$), and p53 was evaluated by Reverse transcription polymerase chain reaction (RT-PCR). Results: The expression of ssrA in a single culture of WT K-12 was lower than that observed in the mixed culture of WT K-12 with S. aureus. Greater ssrA expression was observed in the mixed culture of WT K-12 with Hep2 than in the single culture of WT K-12. The expression of NF-${\kappa}B$ was higher in the mixed culture of Hep2 with ${\Delta}K$-12 than that in the mixed culture of Hep2 with WT K-12, and was lowest in the single culture of Hep2. The expression of ssrA was higher in the mixed culture of WT K-12 with Hep2 and S. aureus than in the mixed culture of WT K-12 with Hep2. Conclusion: These results suggest that ssrA plays an important role in the mechanism of E. coli adaptation to a new environment.