Systemic LPS exposure suppresses pulsatile LH secretion and impairs hepatic function in goats, accompanied by immune activation and stress responses.

Uterine inflammatory diseases are a major cause of subfertility in both humans and domestic animals. Lipopolysaccharide (LPS) is a key mediator of uterine inflammation and reproductive dysfunction. Although the acute suppressive effects of LPS on the hypothalamic-pituitary-gonadal axis are well documented, its sustained effects under persistent inflammation remain unclear. This study investigated the effects of systemic LPS exposure on reproductive and hepatic function, immune activation, and stress responses in estradiol-treated ovariectomized goats. Animals received either a single intravenous (i.v.) bolus injection of LPS or a continuous i.v. infusion. Serial blood samples were collected for 8 h to evaluate plasma concentrations of LPS, interleukin (IL)-1β, cortisol, and liver enzymes, as well as pulsatile luteinizing hormone (LH) secretion. Rectal temperature increased during the early phase after LPS administration. Plasma LPS concentrations increased several hours after LPS administration, with a biphasic elevation observed during continuous LPS infusion. IL-1β and cortisol increased within 1 h of LPS administration, coinciding with LH pulse suppression and preceding the rise in plasma LPS. Gamma-glutamyltransferase (GGT) increased within 3 h and remained elevated after LPS administration. Aspartate transaminase (AST) increased at the end of the continuous LPS infusion experiment. Systemic LPS administration significantly suppressed pulsatile LH secretion compared with saline treatment. These findings suggest that LPS-driven systemic immune activation and/or stress-related endocrine responses may contribute to suppression of pulsatile LH secretion, and that progressive hepatic dysfunction during continuous LPS exposure may contribute to sustained circulating LPS and prolonged reproductive dysfunction.