title: LPS-induced inflammation potentiates the IL-1β-mediated reduction of LH secretion from the anterior pituitary explants.
abstract: Acting at the level of the brain, interleukin- (IL-)1 β is considered to be one of the most potent downregulators of reproduction processes during immune/inflammatory challenge. IL-1 β suppresses gonadotropin-releasing hormone (GnRH) secretion from the hypothalamus resulting in the inhibition of the luteinizing hormone (LH) release from the anterior pituitary (AP). However, the presence of IL-1 β receptors in the AP suggests the possible direct action of this cytokine on LH secretion. The study was designed to determine the effect of IL-1 β on the LH secretion from the AP explants collected from saline and LPS-treated ewes in the follicular phase. It was found that IL-1 β suppressed (P ≤ 0.01) GnRH-stimulated LH release and LH β gene expression in AP explants in both groups. However, IL-1 β action was more potent in the explants collected from LPS-treated animals. Pituitaries from LPS-treated animals were characterized by increased (P ≤ 0.01) IL-1 type I receptor and decreased (P ≤ 0.01) GnRH receptor gene expression level compared to the saline-treated group. IL-1 β also affected the GnRH-R gene expression in explants collected from LPS-treated animals. Our results show that direct action of IL-1 β on the pituitary gonadotropes could be one of the reasons of the reproductive processes disorders accompanying an inflammatory state.
authors: Polish Academy of Sciences, The Kielanowski Institute of Animal Physiology and Nutrition, 05-110 Jabłonna, Poland. a.herman@ifzz.pan.pl
authors: Andrzej Przemysław
authors: AP
authors: Herman
authors: Agata
authors: A
authors: Krawczyńska
authors: Joanna
authors: J
authors: Bochenek
authors: Elżbieta
authors: E
authors: Dobek
authors: Anna
authors: A
authors: Herman
authors: Dorota
authors: D
authors: Tomaszewska-Zaremba
mesh_terms: D000818:Animals; D005786:Gene Expression Regulation / Q000187:drug effects; D007249:Inflammation / Q000139:chemically induced / Q000235:genetics / Q000276:immunology* / Q000378:metabolism*; D053583:Interleukin-1beta / Q000378:metabolism* / Q000494:pharmacology; D008070:Lipopolysaccharides / Q000276:immunology*; D007986:Luteinizing Hormone / Q000235:genetics / Q000378:metabolism*; D010903:Pituitary Gland, Anterior / Q000276:immunology* / Q000378:metabolism* / Q000637:transplantation; D053573:Receptors, Interleukin-1 Type I / Q000235:genetics / Q000378:metabolism; D011966:Receptors, LHRH / Q000235:genetics / Q000378:metabolism
chemical_list: D053583:Interleukin-1beta; D008070:Lipopolysaccharides; D053573:Receptors, Interleukin-1 Type I; D011966:Receptors, LHRH; D007986:Luteinizing Hormone
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