IL-1β immunoreactive neurons in the human hypothalamus:: reduced numbers in multiple sclerosis

IL-1β immunoreactive neurons in the human hypothalamus:: reduced numbers in multiple sclerosis
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DOI:
10.1016/s0165-5728(00)00248-4
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发表时间:
2000-07-10
影响因子:
3.3
通讯作者:
Swaab, D
Swaab, D
中科院分区:
医学4区
文献类型:
--
作者:
Huitinga, I;van der Cammen, M;Swaab, D

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多发性硬化症 (MS) 患者下丘脑室旁核 (PVN) 中含有促肾上腺皮质激素释放激素 (CRH) 的神经元过度活跃。由于白细胞介素-1 (IL-1)β 是 CRH 神经元的强大激活剂,因此在 MS 患者 (n=11) 和匹配对照 (n=11) 的死后下丘脑中研究了其免疫组织化学表达。 10/11 MS 患者的下丘脑组织显示脱髓鞘病变,在许多情况下含有 IL-1 β 免疫反应性 (ir) 巨噬细胞和神经胶质细胞。在对照受试者中,IL-1 beta-ir 仅零星地在神经胶质细胞中发现。有趣的是,下丘脑神经元中也存在丰富的 IL-1 beta-ir。神经元 IL-1 β 与催产素共定位,而不与加压素或 CRH 共定位。 IL-1β 明显在神经元中产生较弱的染色,并且在 MS 中,PVN 中的 IL-1-ir 神经元数量减少了 4.5 倍。我们认为,MS 患者下丘脑中活化的胶质细胞产生的 IL-1β 可能有助于下丘脑 CRH 神经元的激活,而 MS 患者中神经元 IL-1β 表达的减少可能会对神经内分泌、行为或自主功能产生影响。 (C) 2000 Elsevier Science B.V. 保留所有权利。
Corticotropin-releasing hormone (CRH)-containing neurons in the paraventricular nucleus (PVN) in the hypothalamus of multiple sclerosis (MS) patients are hyperactivated. Since interleukin-1 (IL-1)beta is a powerful activator of CRH neurons, its immunohistochemical expression was studied in the postmortem hypothalamus of MS patients (n=11) and matched controls (n=11). Hypothalamic tissue of 10/11 MS patients showed demyelinating lesions that in many cases contained IL-1 beta-immunoreactive (ir) macrophages and glial cells. In control subjects IL-1 beta-ir was only sporadically found in glial cells. Interestingly, abundant IL-1 beta-ir was also present in hypothalamic neurons. Neuronal IL-1 beta co-localised with oxytocin and not with vasopressin or CRH. IL-1 beta clearly yielded a less intense staining in neurons and numbers of IL-1-ir neurons in the PVN were 4.5-fold reduced in MS. We suggest that IL-1 beta produced by activated glial cells in the hypothalamus of MS patients may contribute to the activation of the hypothalamic CRH neurons, while reduced expression of neuronal IL-1 beta in MS patients may have consequences for neuroendocrine, behavioural or autonomic functioning. (C) 2000 Elsevier Science B.V. All rights reserved.