Citation

Huffman EE, Dong BE, Clarke HA, Young LEA, Gentry MS, Allison DB, Sun RC, Waters CM, Alilain WJ. Brain Commun. 2023; 5(2): fcad091.

Copyright

(Copyright © 2023, Oxford University Press)

DOI

10.1093/braincomms/fcad091

PMID

37065091

PMCID

PMC10090796

Abstract

High-cervical spinal cord injury often disrupts respiratory motor pathways and disables breathing in the affected population. Moreover, cervically injured individuals are at risk for developing acute lung injury, which predicts substantial mortality rates. While the correlation between acute lung injury and spinal cord injury has been found in the clinical setting, the field lacks an animal model to interrogate the fundamental biology of this relationship. To begin to address this gap in knowledge, we performed an experimental cervical spinal cord injury (N = 18) alongside sham injury (N = 3) and naïve animals (N = 15) to assess lung injury in adult rats. We demonstrate that animals display some early signs of lung injury two weeks post-spinal cord injury. While no obvious histological signs of injury were observed, the spinal cord injured cohort displayed significant signs of metabolic dysregulation in multiple pathways that include amino acid metabolism, lipid metabolism, and N-linked glycosylation. Collectively, we establish for the first time a model of lung injury after spinal cord injury at an acute time point that can be used to monitor the progression of lung damage, as well as identify potential targets to ameliorate acute lung injury.

Language: en

Keywords

spinal cord injury; lung injury; metabolism