Td. Braden et al., EFFECTS OF INTERLEUKINS ON SECRETION OF LUTEINIZING-HORMONE FROM OVINE PITUITARY-CELLS, American journal of veterinary research, 59(11), 1998, pp. 1488-1493
Objective-To determine whether cytokines of homologous species might m
ediate the stimulatory effects of endotoxin on release of luteinizing
hormone (LH) from pituitary cells. Sample Population-Cells from pituit
ary glands collected from 8- to 14-month-old wethers. Procedure-Cells
from the anterior pituitary gland were cultured in the presence of rec
ombinant ovine or bovine cytokines (interleukin [IL]-1 alpha, IL-1 bet
a, and IL-2), tumor necrosis factor-alpha (TNF), and interferon-gamma
(IFN-gamma). Luteinizing hormone that was released into the medium was
measured. Cells were also cultured with modulators of signal transduc
tion pathways to evaluate the second messenger system used by IL-1 alp
ha and IL-1 beta. Results-Similar to effects of endotoxin, IL-1 alpha
and IL-1 beta stimulated release of LH. Interleukin 2, TNF, and IFN-ga
mma did not have a detectable effect on release of LH. Stimulation of
LH release by IL-1 alpha and IL-1 beta required activation of voltage-
dependent Ca2+ channels and appeared to involve protein kinase C. Conc
lusions-IL-1 alpha and IL-1 beta may mediate the direct stimulatory ef
fect of endotoxin on release of LH in vitro. Interleukin 2, TNF, and I
FN-gamma do not have a direct effect on release of LH; therefore, they
do not mediate this effect of endotoxin. Clinical Relevance-Stressors
, including infection, are often associated with reduced fertility. In
fection resulting in endotoxin release, production of interleukins, or
both, can lead to direct stimulation of LH release from the pituitary
gland. Inopportune release of LH via cytokines may interfere with nor
mal pulsatile release of LH, thereby suppressing gonadal function.