Braden T D, Fry C, Sartin J L
Department of Anatomy, Physiology, and Pharmacology, College of Veterinary Medicine, Auburn University, AL 36849, USA.
Am J Vet Res. 1998 Nov;59(11):1488-93.
To determine whether cytokines of homologous species might mediate the stimulatory effects of endotoxin on release of luteinizing hormone (LH) from pituitary cells.
Cells from pituitary glands collected from 8- to 14-month-old wethers.
Cells from the anterior pituitary gland were cultured in the presence of recombinant ovine or bovine cytokines (interleukin [IL]-1alpha, IL-1beta, 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 transduction pathways to evaluate the second messenger system used by IL-1 alpha and IL-1beta.
Similar to effects of endotoxin, IL-1alpha and IL-1beta stimulated release of LH. Interleukin 2, TNF, and IFN-gamma did not have a detectable effect on release of LH. Stimulation of LH release by IL-1alpha and IL-1beta required activation of voltage-dependent Ca2+ channels and appeared to involve protein kinase C.
IL-1alpha and IL-1beta may mediate the direct stimulatory effect of endotoxin on release of LH in vitro. Interleukin 2, TNF, and IFN-gamma do not have a direct effect on release of LH; therefore, they do not mediate this effect of endotoxin.
Stressors, including infection, are often associated with reduced fertility. Infection 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 normal pulsatile release of LH, thereby suppressing gonadal function.
确定同源物种的细胞因子是否可能介导内毒素对垂体细胞释放促黄体生成素（LH）的刺激作用。
从8至14月龄公羊采集的垂体细胞。
将垂体前叶细胞在重组绵羊或牛细胞因子（白细胞介素[IL]-1α、IL-1β和IL-2）、肿瘤坏死因子-α（TNF）和干扰素-γ（IFN-γ）存在的情况下进行培养。测量释放到培养基中的促黄体生成素。细胞还与信号转导途径调节剂一起培养，以评估IL-1α和IL-1β所使用的第二信使系统。
与内毒素的作用相似，IL-1α和IL-1β刺激LH的释放。白细胞介素2、TNF和IFN-γ对LH的释放没有可检测到的影响。IL-1α和IL-1β刺激LH释放需要电压依赖性Ca2+通道的激活，并且似乎涉及蛋白激酶C。
IL-1α和IL-1β可能介导内毒素在体外对LH释放的直接刺激作用。白细胞介素2、TNF和IFN-γ对LH的释放没有直接影响；因此，它们不介导内毒素的这种作用。
包括感染在内的应激源通常与生育力降低有关。导致内毒素释放、白细胞介素产生或两者兼有的感染可导致垂体直接刺激LH释放。通过细胞因子不恰当地释放LH可能会干扰LH的正常脉冲式释放，从而抑制性腺功能。
