Rol de la prolactina en la prostatitis en ratas

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Endocrinology 144(5):2046 –2054 Copyright © 2003 by The Endocrine Society doi: 10.1210/en.2002-0038

The Role of Prolactin in the Prostatic Inflammatory Response to Neonatal Estrogen
JASON P. GILLERAN*, OLIVER PUTZ*, MEGAN DEJONG, SAMUEL DEJONG, LYNN BIRCH, YONGBING PU, LIWEI HUANG, AND GAIL S. PRINS
Department of Urology, College of Medicine, University of Illinois at Chicago, Chicago, Illinois 60612
Estrogen exposure in the neonatal rat has been shown to disrupt the normal morphology and development of the prostate gland. The response to this exposure is manifest in adulthood as epithelial dysplasia and chronic inflammation. This inflammatory response consists of infiltrating T-lymphocytes
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chronic inflammation of that organ (11–14). Thus, the young adult and aged estrogenized prostates are characterized by the presence of luminal granulocytes, marked stromal macrophage infiltration, and mild-to-severe lymphocytic aggregation within the stromal compartment with diapedisis across the epithelium as the animals age. This is noteworthy in that persistent inflammation has been observed in diseases of the human prostate including benign prostatic hyperplasia and adenocarcinoma and a causal relationship has been suggested (15, 16). The basis for the chronic inflammatory response in the neonatally estrogenized prostate is not understood. However, it is known that both estrogens and PRL can have marked effects on the immune system in general and prostatic inflammation in particular. It is established that estrogens stimulate anterior pituitary PRL secretion through inhibition of hypothalamic dopaminergic suppression pathways (17). Thus, exogenous estrogenic exposures result in relative hyperprolactinemia for variable lengths of time (18, 19). Importantly, estrogeninduced hyperprolactinemia in the adult rat has been shown to induce prostatitis (20). Recently, Stoker and colleagues (21, 22) have shown that elevations in circulating PRL during

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