The vagus nerve-dependent lung-brain axis mediates brain demyelination following acute lung injury

IF 3.5 Q2 IMMUNOLOGY Brain, behavior, & immunity - health Pub Date : 2025-02-11 DOI:10.1016/j.bbih.2025.100966

Dan Xu , Mingming Zhao , Guilin Liu , Tingting Zhu , Yi Cai , Rumi Murayama , Yong Yue , Kenji Hashimoto

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Abstract

Patients with acute lung injury (ALI) often experience psychiatric and neurological symptoms; however, the precise underlying mechanisms remain unclear. Given that white matter loss (demyelination) contributes to these symptoms, we investigated whether lipopolysaccharide (LPS)-induced ALI leads to brain demyelination via a vagus nerve-dependent lung-brain axis. A single intratracheal injection of LPS caused severe lung injury and demyelination in the corpus callosum (CC) of mouse brains. Subdiaphragmatic vagotomy did not affect LPS-induced lung injury or demyelination in the CC. Interestingly, cervical vagotomy significantly attenuated LPS-induced hypo-locomotion, plasma interleukin-6 levels, and demyelination in the CC of ALI mice without influencing lung injury. These findings demonstrate that ALI can induce demyelination in the CC of the mouse brain via a cervical vagus nerve-dependent lung-brain axis, highlighting the critical role of this pathway in the psychiatric and neurological symptoms observed in ALI patients.

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迷走神经依赖的肺脑轴介导急性肺损伤后的脑脱髓鞘

急性肺损伤（ALI）患者常出现精神和神经系统症状；然而，确切的潜在机制仍不清楚。鉴于白质损失（脱髓鞘）有助于这些症状，我们研究了脂多糖（LPS）诱导的ALI是否通过迷走神经依赖的肺-脑轴导致脑脱髓鞘。单次气管内注射LPS可引起小鼠脑胼胝体（CC）严重的肺损伤和脱髓鞘。膈下迷走神经切断术不影响lps诱导的CC肺损伤或脱髓鞘，有趣的是，颈迷走神经切断术显著减轻lps诱导的ALI小鼠CC运动障碍、血浆白细胞介素-6水平和脱髓鞘，但不影响肺损伤。这些发现表明，ALI可以通过颈迷走神经依赖的肺-脑轴诱导小鼠脑CC脱髓鞘，突出了该途径在ALI患者观察到的精神和神经症状中的关键作用。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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