脑室内出血是一种可能危及生命的疾病。大约20%的患者会出现出血后脑积水，并伴有脑室容积和颅内压增加。脑积水的发生部分是由于脉络丛脑脊液分泌增加所致。出血期间，多种因子被释放到脑脊液中。其中许多与分泌过多有关。在这项研究中，我们研究了炎症成分对参与脉络丛脑脊液分泌的两种膜转运蛋白丰度的单独影响：Na 依赖性 Cl-/HCO3- 交换器 Ncbe 和 Na 、 K 、 2Cl-协同转运蛋白，NKCC1。我们建立了 1 至 7 天龄小鼠幼仔的原代脉络丛上皮细胞培养物。接种7天后，细胞形成单层。这些细胞用肿瘤坏死因子 α (TNFα)、白细胞介素 1 β (IL-1β) 或白细胞介素 6 (IL-6) 处理以模拟炎症。数据显示，用 TNFα 和 IL-1β 处理仅短暂增加 NKCC1 丰度，而对 Ncbe 丰度的影响是短暂降低。然而，IL-6 显着增加 NKCC1 (242%)、磷酸化 NKCC1 (147%) 以及 pSPAK (406%) 丰度，但对 Ncbe 没有影响。这项研究表明，分泌过多所涉及的炎症途径主要是由脉络丛中基底外侧受体的激活介导的，主要由 IL-6 促进。这项研究强调了脑室内出血期间发生的病理生理情况的复杂性。© 2023。BioMed Central Ltd.，Springer Nature 旗下公司。

Intraventricular hemorrhage is a potentially life-threatening condition. Approximately 20% of patients develop posthemorrhagic hydrocephalus with increased ventricular volume and intracranial pressure. Hydrocephalus develops partially due to increased secretion of cerebrospinal fluid by the choroid plexus. During hemorrhage a multitude of factors are released into the cerebrospinal fluid. Many of these have been implicated in the hypersecretion. In this study, we have investigated the isolated effect of inflammatory components, on the abundance of two membrane transporters involved in cerebrospinal fluid secretion by the choroid plexus: the Na+-dependent Cl-/HCO3- exchanger, Ncbe, and the Na+, K+, 2Cl- cotransporter, NKCC1. We have established a primary choroid plexus epithelial cell culture from 1 to 7 days old mouse pups. Seven days after seeding, the cells formed a monolayer. The cells were treated with either tumor necrosis factor alpha (TNFα), interleukin 1 beta (IL-1β), or interleukin 6 (IL-6) to mimic inflammation. The data show that treatment with TNFα, and IL-1β only transiently increased NKCC1 abundance whereas the effect on Ncbe abundance was a transient decrease. IL-6 however significantly increased NKCC1 (242%), the phosphorylated NKCC1 (147%), as well as pSPAK (406%) abundance, but had no effect on Ncbe. This study suggests that the inflammatory pathway involved in hypersecretion primarily is mediated by activation of basolateral receptors in the choroid plexus, mainly facilitated by IL-6. This study highlights the complexity of the pathophysiological circumstances occurring during intraventricular hemorrhage.© 2023. BioMed Central Ltd., part of Springer Nature.