Inhibition of p53 alleviates prostate cell apoptosis in Escherichia coli‑induced bacterial prostatitis

Previous studies demonstrated that uropathogenic Escherichia coli infection contributes to human bacterial prostatitis. Apoptosis of prostate epithelial cells is closely associated with the progression of bacterial prostatitis. The aim of the present study was to investigate the effect of cellular tumor antigen p53 (p53) on the apoptosis of bacterial prostatitis cells. The prostate epithelial RWPE‑1 cell line was infected with Escherichia coli, and treated cells and the culture supernatant were obtained at specific time points. The cell apoptosis rates, protein and mRNA of p53 were detected in the different treatment groups. Flow cytometry and terminal deoxynucleotidyl‑transferase‑mediated dUTP nick end labeling assays were used for the detection of cell apoptosis, and cell proliferation was determined by a Cell Counting Kit‑8 assay. The expression of p53 was inhibited by small interfering (si)RNA, and its mRNA and protein were detected. An ELISA was used for detecting cytokines in the culture supernatant. The result demonstrated that Escherichia coli infection led to an increase in prostate epithelial cell apoptosis (P<0.05), and resulted in increases of interleukin (IL)‑4, IL‑6 and IL‑8, and decrease in IL‑10. p53, apoptosis regulator BAX (Bax), caspase‑9 and Caspase‑3 expression were upregulated upon Escherichia coli exposure (P<0.05). Following transfection with p53 siRNA, the promotion of cell apoptosis induced by Escherichia coli infection was decreased, and the p53 and Bax protein expression were additionally decreased. Therefore, it was suggested that Escherichia coli increases cell apoptosis in bacterial prostatitis by activating the death receptor pathway involving p53. Inhibition of p53 alleviated prostate cell apoptosis induced by Escherichia coli.