Immunological, structural, and functional changes of spinal cord injury-associated pneumonia (SCI-AP)
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Date
2024-05
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The Ohio State University
Abstract
Background: SCI-associated pneumonia (SCI-AP) is an outcome modifier associated with increased mortality and disability. The underlying pathophysiology of the SCI-associated pneumonia (SCI-AP) in the lung has not yet been established. We hypothesise that acute SCI-AP cause long-term changes in the lung.
Methods: Using a clinically relevant controlled model of induced SCI-AP, structural, immunological, and functional changes were monitored and quantified comparing SCI-AP with SCI-only groups. Matching clinical onset, SCI-AP was induced by inoculating the mice with D39 Streptococcus pneumoniae at 3 days post-injury (500 CFU or 5000 CFU). All histopathological assessments were performed at acute and chronic timepoints post-injury. The presence of bacteria in the bronchioles of the lung tissue was assessed with a Streptococcus pneumoniae antibody and emerging structural changes in bronchial wall thickness and apoptosis of bronchioles were assessed in the lower right lung. Lung inflammation was assessed with flow cytometry to measure additional changes in immune cell markers.
Results: SCI-AP increases apoptosis and inflammation in the lung compared to SCI alone. Functionally, mice with acquired pneumonia have impaired respiration compared to SCI only mice, as early as 12 hours after inoculation. Overall, this work demonstrates features of acute and chronic SCI-AP and its subsequent structural, immunological, and functional changes in the lung.
Interpretation: These results indicate that SCI-AP evokes damage to the lung tissue and decreases overall lung function lasting beyond the acute SCI phase. Moreover, they provide new insights and characterize an animal SCI-AP model applicable to develop effective therapeutics and/or prevention methods for patients suffering from SCI-induced immunosuppression.
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Keywords
Spinal Cord Injury, Infection, Lung Damage, Immunohistochemistry