Abstract
Acting at the level of the brain, interleukin- (IL-)1β is considered to be one of the most potent downregulators of reproduction processes during immune/inflammatory challenge. IL-1β 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-1β 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-1β on the LH secretion from the AP explants collected from saline and LPS-treated ewes in the follicular phase. It was found that IL-1β suppressed (P ≤ 0.01) GnRH-stimulated LH release and LHβ gene expression in AP explants in both groups. However, IL-1β 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-1β also affected the GnRH-R gene expression in explants collected from LPS-treated animals. Our results show that direct action of IL-1β on the pituitary gonadotropes could be one of the reasons of the reproductive processes disorders accompanying an inflammatory state.
Highlights
An immune/inflammatory challenge is considered as an important factor inhibiting the reproduction process in animals and human
Numerous in vitro and in vivo studies showed that the immune stress affects the gonadotropin-releasing hormone (GnRH)/luteinizing hormone (LH) secretion by the central action of proinflammatory cytokines affecting the secretory activity of GnRH neurons in the hypothalamus [4,5,6]
In the explants collected from saline and LPS-treated ewes, the GnRH significantly (P ≤ 0.01) stimulated LH release, and there were no important differences in their response to GnRH (Figure 1)
Summary
An immune/inflammatory challenge is considered as an important factor inhibiting the reproduction process in animals and human. The inflammation caused by peripheral administration of bacterial endotoxin-lipopolysaccharide (LPS) significantly decreases gonadotropin-releasing hormone (GnRH) and luteinizing hormone (LH) secretion [1,2,3]. These interconnections existing between the immune and the neuroendocrine systems are based on the mutual sharing of receptors and mediators [4]. Its action at the level of the hypothalamus is considered as an important mechanism via inflammation downregulates GnRH/LH secretion [8,9,10]. The presence of IL-1 type I receptor (IL-1R1) in the pituitary [11, 12] suggests that antigonadotropic action of IL-1β could be more complex and may occur at the level of this gland
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