The vagus nerve-dependent lung-brain axis mediates brain demyelination following acute lung injury
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 b...
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| Main Authors: | , , , , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Elsevier
2025-03-01
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| Series: | Brain, Behavior, & Immunity - Health |
| Subjects: | |
| Online Access: | http://www.sciencedirect.com/science/article/pii/S2666354625000249 |
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| Summary: | 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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| ISSN: | 2666-3546 |