Mechanical Ventilation Modulates Pro-Inflammatory Cytokine Expression in Spinal Cord Tissue After Injury in Rats
Rationale: Spinal cord injury (SCI) may induce significant respiratory muscle weakness and paralysis, which in turn may cause a patient to require ventilator support. Central nervous system alterations can also exacerbate local inflammatory responses with immune cell infiltration leading to additional risk of inflammation at the injury site. Although mechanical ventilation is the traditional treatment for respiratory insufficiency, evidence has shown that it may directly affect distant organs through systemic inflammation. Objectives: This study aimed to better understand the impact of invasive mechanical ventilation on local spinal cord inflammatory responses following cervical or thoracic SCI. Methods: Five groups of female Sprague-Dawley rats were anesthetised for 24 h. Three groups received mechanical ventilation: seven rats without SCI, seven rats with cervical injury (C4-C5), and seven rats with thoracic injury (T10); whereas, two groups were non-ventilated: six rats without SCI; and six rats with thoracic injury (T10). Changes in inflammatory responses were determined in the spinal cord tissues collected at the local site of injury. Cytokines were measured using ELISA. Main results: SCI induced local pro-inflammatory cytokine IL-6 expression for all groups. Mechanical ventilation also had effects on pro-inflammatory cytokines and independently increased TNF-α and decreased IL-1β levels in the spinal cords of anesthetized rats. Conclusion: These data provide the first evidence that mechanical ventilation contributes to local inflammation after SCI and in the absence of direct tissue injury.
Truflandier, Karine; Beaumont, Eric; Charbonney, Emmanuel; Maghni, Karim; de Marchie, Michel; and Spahija, Jadranka. 2018. Mechanical Ventilation Modulates Pro-Inflammatory Cytokine Expression in Spinal Cord Tissue After Injury in Rats. Neuroscience Letters. Vol.671 13-18. https://doi.org/10.1016/j.neulet.2018.01.028 PMID: 29355694 ISSN: 0304-3940