Increasing evidence suggests an important role of epithelial cells (EC) in the innate immune host defense. Whereas some anatomical sites preserve a sterile environment, like the prostate, most surfaces are colonized by a diverse microflora and have evolved to distinguish between normal or pathogenic microorganisms.
Since E. Coli is one of the most common causes of infection of the prostate gland by ascending bacteria from infected urine, we wanted to know if prostatic EC have an LPS responsive phenotype that could facilitate the detection of bacteria at early stages of infection.
The rat prostatic epithelial cell line JHU-4 was stimulated by 100 ug of E coli 055:B5 LPS for 6, 24 and 48 hours. The expression of TLR2, TLR4 and the chemokines IL8, RANTES, IP10, MCP-1, MP1a, MIP1b were evaluated by RT-PCR.
Stimulation of JHU cells with bacterial LPS induced a significant increase in the mRNA levels of RANTES, IP10 ,MCP1, MIP-1a and MIP1b that could be easily identified 6h post stimulation. Although we could detect expression of IL8 in non stimulated JHU cells, it showed a two fold increase after 24h of the addition of LPS.
Interestingly, the expression of TLR2 mRNA was not detected in non stimulated cells but it was induced after 6h of culture with LPS. In contrast, basal levels of TLR4 mRNA was readily detected in non stimulated cells, but a strong enhancement of its expression was observed after LPS stimulation, reaching maximum expression 24h after stimulation.
We show for the first time that prostatic epithelial cells express TLR2 and TLR4 in an inducible manner and are susceptible to LPS stimulation expressing a wide spectrum of chemokines that could facilitate the initiation of an inflammatory response.
