Endotoxin rapidly desensitizes the gonads to kisspeptin-induced luteinizing hormone release in male Siberian hamsters (Phodopus sungorus) [RESEARCH ARTICLE]

Kimberly L. P. Long, Allison M. Bailey, Timothy J. Greives, Sandra J. Legan, and Gregory E. Demas

Activation of the immune system induces rapid reductions in hypothalamic-pituitary-gonadal (HPG) axis activity, which in turn decreases secretion of sex steroids. This response is likely adaptive for survival by temporarily inhibiting reproduction to conserve energy; however, the physiological mechanisms controlling this response remain unclear. The neuropeptide kisspeptin is a candidate to mediate the decrease in sex hormones seen during sickness through its key regulation of the HPG axis. In this study, the effects of acute immune activation on the response to kisspeptin were assessed in male Siberian hamsters (Phodopus sungorus). Specifically, an immune response was induced in animals by a single treatment of lipopolysaccharide (LPS), and reproductive hormone concentrations were determined in response to subsequent injections of exogenous kisspeptin. Saline-treated controls showed a robust increase in circulating testosterone in response to kisspeptin; however, this response was blocked in LPS-treated animals. Circulating luteinizing hormone (LH) levels were elevated in response to kisspeptin in both LPS- and saline-treated groups and, thus, were unaffected by LPS treatment, suggesting gonad-level inhibition of testosterone release despite central HPG activation. In addition, blockade of glucocorticoid receptors by mifepristone did not attenuate the LPS-induced inhibition of testosterone release, suggesting that circulating glucocorticoids do not mediate this phenomenon. Collectively, these findings reveal that acute endotoxin exposure rapidly renders the gonads less sensitive to HPG stimulation, thus effectively inhibiting sex hormone release. More broadly, these results shed light on the effects of immune activation on the HPG axis and help elucidate the mechanisms controlling energy allocation and reproduction.

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