孕期暴露于酒精会减弱大鼠脾脏对内毒素和白细胞介素-1β的交感神经反应。
Exposure to alcohol in utero blunts splenic sympathetic neural response to endotoxin and interleukin-1beta in the rat.
作者信息
Gottesfeld Z, Simpson S, Maier M
机构信息
Department of Neurobiology and Anatomy, University of Texas Medical School, Houston 77225, USA.
出版信息
J Neuroimmunol. 1997 Sep;78(1-2):180-3. doi: 10.1016/s0165-5728(97)00099-4.
Systemic administration of endotoxin (LPS) or interleukin-1beta (IL-1) to prepubertal rats induced a marked increase in splenic but not cardiac norepinephrine (NE) turnover, an index of sympathetic neural activity. In contrast, the splenic neural response was blunted in their fetal alcohol-exposed (FAE) cohorts. Because the sympathetic outflow to lymphoid organs is considered an important immune modulator, the anomalous neural response to immune signals may partly account for the impaired cellular immunity and, thus, for the increased susceptibility to infections associated with FAE.
对青春期前大鼠进行内毒素（LPS）或白细胞介素-1β（IL-1）的全身给药，会导致脾脏而非心脏去甲肾上腺素（NE）周转率显著增加，NE周转率是交感神经活动的一个指标。相比之下，在胎儿酒精暴露（FAE）组中，脾脏神经反应减弱。由于流向淋巴器官的交感神经输出被认为是一种重要的免疫调节因子，对免疫信号的异常神经反应可能部分解释了细胞免疫受损的原因，进而解释了与FAE相关的感染易感性增加的原因。
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