How does bacterial endotoxin influence gonadoliberin/gonadotropins secretion and action?

Abstract

This review summarizes data concerning the mechanisms by which bacterial endotoxin, lipopolysaccharide (LPS), inhibits gonadoliberin (GnRH)/ luteinizing hormone (LH) secretion in mammals. LPS is a major component of Gram-negative bacteria cell walls and is released from the surface of replicated and dying Gram-negative bacteria into circulation. LPS is commonly used to induce immune/inflammatory challenge in animals. In this article the site of endotoxin action as well as LPS induced mediators are discussed. Hypothalamus seems to be a place where majority of the immune-neuroendocrine interactions occur, however the results of many research suggest that LPS may interfere with reproductive system at the pituitary level as well. Endotoxin may affect GnRH/LH secretion directly via toll-like receptors (TLR)4/TLR2 located both in the hypothalamus and pituitary or indirectly through the intermediates such as cytokines, catecholamines, prostaglandins or opioids.