Prolactin and lipopolysaccharide treatment increased apoptosis and atresiain rat ovarian follicles

Follicular atresia is associated with the presence of increased macrophages within the follicle. What is not known is whether, in the adult rat, macro phages are instrumental in inducing apoptosis and/or atresia or whether the y are simply secondary to a hormonally mediated event. As prolactin is an i mmunoreactive hormone and stimulates the expression of monocyte chemoattrac tant, the present experiments compared the effects of prolactin treatment w ith that of an immune challenge with lipopolysaccharide (LPS) on the invasi on of macrophages into the follicular and luteal compartments of the ovary and the occurrence of apoptosis/atresia in relation to macrophage invasion. Rats were treated for 3 days with either prolactin or LPS and ovaries obta ined at pro-oestrus or oestrus. Prolactin and LPS increased the number of a tretic vs. healthy follicles (P < 0.008, <chi>(2)) in pro-oestrus ovaries a nd increased the mean number of apoptotic cells and macrophages (P < 0.05 f or some groups). Macrophages were typically observed in the thecal layer, a poptotic cells in the granulosa cell layer, although 84% follicles which ha d macrophages within the granulosa cell layer also contained relatively hig h numbers of apoptotic nuclei. Prolactin and LPS treatment in vivo reduced the progesterone response to follicle stimulating hormone (FSH) (P < 0.001) in cultures of ovarian dispersates but did not inhibit the response to for skolin. In contrast, prolactin or LPS added in vitro to the cultures inhibi ted the progesterone response to forskolin. Results shaw that both prolacti n and LPS increase follicular apoptosis and atresia and reduce the progeste rone response to FSH.