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Abstract
BackgroundImmune stress induced by lipopolysaccharide (LPS) influences the gonadotropin-releasing hormone (GnRH)/luteinizing hormone (LH) secretion. Presence of LPS interacting Toll-like receptor (TLR) 4 in the hypothalamus may enable the direct action of LPS on the GnRH/LH secretion. So, the aim of the study was to investigate the influence of intracerebroventricular (icv) injection of TLR4 antagonist on GnRH/LH secretion in anestrous ewes during LPS-induced central inflammation. Animals were divided into three groups icv-treated with: Ringer-Locke solution, LPS and TLR4 antagonist followed by LPS.ResultsIt was demonstrated that TLR4 antagonist reduced LPS-dependent suppression of GnRH gene expression in the preoptic area and in the medial basal hypothalamus, and suppression of receptor for GnRH gene expression in the anterior pituitary gland. It was also shown that TLR4 antagonist reduced suppression of LH release caused by icv injection of LPS. Central administration of LPS stimulated TLR4 gene expression in the medial basal hypothalamus.ConclusionsIt was indicated that blockade of TLR4 prevents the inhibitory effect of centrally acting LPS on the GnRH/LH secretion. This suggests that some negative effects of bacterial infection on the hypothalamic-pituitary-gonadal axis activity at the hypothalamic level may be caused by central action of LPS acting through TLR4.
Highlights
Immune stress induced by lipopolysaccharide (LPS) influences the gonadotropin-releasing hormone (GnRH)/luteinizing hormone (LH) secretion
Treatment with CD14/TLR4 antagonist reduced the inhibitory effect of LPS on LH release (Fig. 1a)
Effect of icv administration of CD14/TLR4 antagonist on GnRH synthesis in the median eminence (ME) during central inflammation induced by icv administration of LPS Centrally administered LPS decreased (P < 0.05) GnRH concentration in the ME as compared with control group
Summary
Immune stress induced by lipopolysaccharide (LPS) influences the gonadotropin-releasing hormone (GnRH)/luteinizing hormone (LH) secretion. Presence of LPS interacting Toll-like receptor (TLR) 4 in the hypothalamus may enable the direct action of LPS on the GnRH/LH secretion. LPS induces cellular responses through Toll-like receptor (TLR) 4, that plays a crucial role in the activation of innate immunity and pathogen recognition [5, 6]. Animal cells are stimulated by LPS through signaling cascades with several specific proteins like cluster of differentiation (CD) 14 protein, myeloid differentiation factor 2 (MD-2) and LPS-binding protein (LBP), a necessary component of TLR4 [7, 8]. Endotoxin forms a Haziak et al Journal of Animal Science and Biotechnology (2018) 9:52 complex with LBP, and this complex binds to CD14, which plays a pivotal role in TLR4 receptor activation [9, 10]. In collaboration with these proteins, TLR4 is activated and can conduct its inflammatory signal through the system of intracellular pathways, which leads to activation of some transcription factors or induces apoptosis [11, 12]
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