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AUTOIMMUNITY AS A POSSIBLE MECHANISM OF PROTACTIN-INDUCED PROSTATITIS
Citation:
Luebke, R W., C B. Copeland, AND L. R. Bishop. AUTOIMMUNITY AS A POSSIBLE MECHANISM OF PROTACTIN-INDUCED PROSTATITIS. Presented at Society of Toxicology, San Francisco, CA, March 25-29,2001.
Description:
AUTOIMMUNITY AS A POSSIBLE MECHANISM OF PROLACTIN-INDUCED PROSTATITIS. RW Luebke, CB Copeland, and LR Bishop. US EPA, Research Triangle Park, NC
Stoker et al. reported inflammation of the lateral prostate (LP) lobes in 120 day old Wistar rats after manipulation of prolactin (PRL) levels during the prepubertal period. The inflammatory response, comprised of intraductal neutrophils plus monocytes within the stroma, is similar to that observed in human nonbacterial prostatitis (NBP). Epidemiologic studies identified an increased risk of prostate cancer in pesticide applicators as well as a higher incidence of NBP. PRL also has potent immunomodulatory properties, including upregulation of TNF and iNOS expression and to stimulate activation of T cells. Hyperprolactinemia has been associated with increased severity of arthritis, SLE and type 1 diabetes, and may be a risk factor for other atoimmune diseases. We tested the hypothesis that specific autoreactivity to LP components causes prostatitis. Male pups were dosed with the dopamine inhibitor pimozide from PND22-32 and sacrificed on PNDs 45, 75 and 120. Circulating antibody to crude LP antigen (LPA )was not observed and LPA did not stimulate proliferation of spleen or draining lymph node cells. However, mRNA for IFN ICAM-1 and MIP-1 were increased by PND45, well before frank inflammation was present.