Effects of LPS on the Secretion of Gonadotrophin Hormones and Expression of Genes in the Hypothalamus-Pituitary-Ovary (HPG) Axis in Laying Yangzhou Geese

Simple Summary Lipopolysaccharide (LPS), an endotoxin from E. coli, has been proven to impair follicle development and steroidogenesis, secretion of pituitary and hypothalamus reproductive hormones in mammals. However, the effects of LPS on the avian reproductive axis remain elusive. Pathogenic bacterial infection due to the particular mating behavior on the water containing pathogens was reported to decrease the laying rate and cause economic loss in goose production. In this study, we showed that LPS infection disturbed the plasma pituitary gonadotrophin hormone concentrations and the gene expression of the reproductive axis in Yangzhou geese. Notably, for the first time we proved that both the expression of gonadotrophin-releasing hormone (GnRH) and gonadotropin-inhibiting hormone (GnIH), two important reproductive genes from the hypothalamus, were altered after LPS treatment in birds. Our results can explain the decreased laying rate in goose after bacterial infection, and also provide new insights into reproductive dysfunction caused by LPS and the immune challenge in birds. Lipopolysaccharide (LPS) from gram-negative bacteria was found to be involved in the decrease in laying performance in goose flocks with high stocking density during summer months. LPS injection delayed the increase in the laying rate and altered hierarchical follicle morphology. While there is evidence that LPS exerts suppressive effects on goose reproduction, the time course effects of LPS on the hypothalamus-pituitary-ovary (HPG) axis remain elusive. In this study, we investigated the expression of genes in the HPG axis and the plasma gonadotrophin hormone concentrations in breeding geese at 0, 6, 12, 24, and 36 h after intravenous injection with LPS. The results showed that LPS treatment enhanced and suppressed expression of hypothalamic gonadotropin-inhibiting hormone (GnIH) and gonadotrophin-releasing hormone (GnRH) mRNA, respectively, and similar effects were observed on the mRNA expression of their receptors, GnIHR and GnRHR, in the pituitary. LPS treatment transiently increased follicle FSH beta mRNA expression at 12 h and exerted no significant effect on LH beta mRNA expression in the pituitary. Regardless of the expression of FSH beta and LH beta, plasma follicle stimulating hormone (FSH) and luteinizing hormone (LH) concentrations were significantly increased during 24-36 h after LPS treatment. In the ovary, StAR and Cyp11a1 were mainly expressed in the granulosa layer (GL) of hierarchical follicles, while Cyp17a1 and Cyp19a1 were mainly expressed in white follicles (WFs) and yellowish follicles (YFs), and to a lesser extent in the theca layer (TL). After LPS treatment, the mRNA levels of Cyp11a1 in the GLs, Cyp17a1 in the WFs and TL, and Cyp19a1 in the WFs, YFs, and TL were significantly decreased. However, LPS treatment transiently upregulated StAR expression at 12 h. These results indicate that the exposure of laying geese to LPS may impair the HPG axis and disturb ovarian steroidogenesis. Our research provides new insights into reproductive dysfunction caused by LPS and the immune challenge in birds.