Login to Access Video or Poster Abstract: MP17-05
Sources of Funding: NIH-NIDDK

Introduction

Inflammation is the most prevalent and widespread histological finding in the human prostate, and associates with the development and progression of benign prostatic hyperplasia. Several factors have been hypothesized to cause inflammation, yet the role each plays in the etiology of prostatic inflammation remains unclear. This study investigated a role for the common protozoan parasite Toxoplasma gondii in prostatic inflammation and established a novel mouse model.

Methods

Male mice were infected intraperitoneally with green fluorescent protein (GFP)-expressing T. gondii parasites and prostatic infection was confirmed with parasite specific staining and GFP localization. The resulting prostatic inflammation was scored on severity and focality of infiltrating leukocytes and epithelial hyperplasia. We characterized inflammatory cells with flow cytometry and the resulting epithelial proliferation with bromodeoxyuridine (BrdU) incorporation. In addition, human sera from T. gondii IgG seropositive and seronegative male patients were tested for total prostate specific antigen (PSA) concentrations by ELISA.

Results

We found that T. gondii infects the mouse prostate during systemic infection and can establish parasite cysts that persist for at least 60 days. T. gondii infection induces a substantial and chronic inflammatory reaction in the mouse prostate characterized by monocytic and lymphocytic inflammatory infiltrate. T. gondii-induced inflammation results in reactive hyperplasia, involving basal and luminal epithelial proliferation, and the exhibition of microglandular hyperplasia in 60 day inflamed mouse prostates. Finally, T. gondii seropositive men have 5.08 times the odds of having an elevated PSA level (>4.0 ng/ml) than age-matched seronegative men.

Conclusions

We found that T. gondii infects the mouse prostate during systemic infection and can establish parasite cysts that persist for at least 60 days. T. gondii infection induces a substantial and chronic inflammatory reaction in the mouse prostate characterized by monocytic and lymphocytic inflammatory infiltrate. T. gondii-induced inflammation results in reactive hyperplasia, involving basal and luminal epithelial proliferation, and the exhibition of microglandular hyperplasia in 60 day inflamed mouse prostates. Finally, T. gondii seropositive men have 5.08 times the odds of having an elevated PSA level (>4.0 ng/ml) than age-matched seronegative men.

Funding

NIH-NIDDK