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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.

plos one

Growth and adherence of Staphylococcus aureus were enhanced through the PGE2 produced by the activated COX-2/PGE2 pathway of infected oral epithelial cells