Growth and adherence of Staphylococcus aureus were enhanced through the PGE(2) produced by the activated COX-2/PGE(2) pathway of infected oral epithelial cells

Staphylococcus aureus is a major pathogen of varieties of oral mucous infection. Prostaglandin E2 (PGE(2)) is a pro-inflammatory factor and Cyclooxygenase 2 (COX-2) is a critical enzyme of PGE(2) biosynthesis. The purpose of this study is to investigate whether Staphylococcus aureus can increase PGE(2) production of oral epithelial cells and how PGE(2) functions in the growth and adherence of Staphylococcus aureus. mRNA levels of COX-2, fnbpA and fnbpB were estimated by quantitative PCR. PGE(2) production was measured by Enzyme Linked Immunosorbent Assay (ELISA). The binding biomass of Staphylococcus aureus to human fibronectin was investigated by crystal violet staining and confocal laser scanning microscopy and the adherent force was measured by atomic force microscope (AFM). The COX-2 mRNA level and PGE(2) production were increased by Staphylococcus aureus. PGE(2) promoted the growth and biofilm formation of Staphylococcus aureus, enhanced the attachment of Staphylococcus aureus to the human fibronectin as well as to the HOK cells. The transcription of fnbpB was up-regulated by PGE(2) in both early and middle exponential phase but not fnbpA. These results suggest that the activation of COX-2/PGE(2) pathway in oral epithelial cell by Staphylococcus aureus can in turn facilitate the growth and the ability to adhere of the pathogen. These findings uncover a new function of PGE(2) and may lead to the potential of COX-2/PGE(2) targeting in the therapy of inflammation and cancer in both which the COX-2/PGE(2) pathway were observed activated.