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

by Yuxia Wang, Biao Ren, Xuedong Zhou, Shiyu Liu, Yujie Zhou, Bolei Li, Yaling Jiang, Mingyun Li, Mingye Feng, Lei Cheng

Staphylococcus aureus is a major pathogen of varieties of oral mucous infection. Prostaglandin E2 (PGE₂) is a pro-inflammatory factor and Cyclooxygenase 2 (COX-2) is a critical enzyme of PGE₂ biosynthesis. The purpose of this study is to investigate whether Staphylococcus aureus can increase PGE₂ production of oral epithelial cells and how PGE₂ functions in the growth and adherence of Staphylococcus aureus. mRNA levels of COX-2, fnbpA and fnbpB were estimated by quantitative PCR. PGE₂ 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 PGE₂ production were increased by Staphylococcus aureus. PGE₂ 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 PGE₂ in both early and middle exponential phase but not fnbpA. These results suggest that the activation of COX-2/PGE₂ 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 PGE₂ and may lead to the potential of COX-2/PGE₂ targeting in the therapy of inflammation and cancer in both which the COX-2/PGE₂ pathway were observed activated.

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