Role Of Bacterial Infection For Innate Immunity On Cells From Prostate Carcinoma And Benign Prostate Hyperplasia

The immunological and cell biological network in prostate carcinoma (CaP) and benign prostate hyperplasia (BPH) with regard to parameters of innate immunity has been recently of major interest. We studied the effect of various common bacterial isolates (n=5), i.e. Staphylococcus aureus, Staphylococcus epidermidis, Enterococcus faecalis, Escherichia coli, Pseudomonas aeruginosa on various prostate carcinoma cells (PC3, LNCAP, DU145) in comparison to a benign prostate hyperplasia cell line (BPH1) over various times (2–48 hours). In addition, the various cell lines (CaP, BPH) were incubated with the bacterial isolates and subsequently stimulated with various growth factors (VEGF, FGF, HGF, EGF, IGF). By Elisa were assessed the supernatants of the target cells for cytokine release (IL6, IL8, TGF-beta, VEGF) as well as PGE2. Parameters of innate immunity for the various cell lines, e.g. Toll-like receptors (2, 4, 9), trefoil peptides (TFF 1–3), receptors for prostaglandin E2 (EP 1–4), proteases (PAR 1–4), cystenylleukotrienes (Cys LTR 1, 2), as well as oxidases (p22, 47, 67, gp91phox) and cyclooxygenase 2 were determined by RT-PCR and/or taqman analysis. Our data indicate that bacteria modulate inflammatory mediator release and parameters of innate immunity depending on the individual strain and cell line and therefore may trigger cell biological and inflammatory responses of CaP/BPH cells for tumour development and progression.