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

IF 3.7 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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