Evaluation and Characterization of Post-Stroke Lung Damage in a Murine Model of Cerebral Ischemia.

Abstract

After stroke and other brain injuries , there is a high incidence of respiratory complications such as pneumonia or acute lung injury . The molecular mechanisms that drive the brain - lung interaction post- stroke have not yet been elucidated. We performed transient middle cerebral artery occlusion (MCAO) and sham surgery on C57BL/6J mice and collected bronchoalveolar lavage fluid (BALF), serum , brain , and lung homogenate samples 24 h after surgery . A 92 proteins -panel developed by Olink Proteomics ® was used to analyze the content in BALF and lung homogenates. MCAO animals had higher protein concentration levels in BALF than sham-controls, but these levels did not correlate with the infarct volume. No alteration in alveolar- capillary barrier permeability was observed. A total of 12 and 14 proteins were differentially expressed between the groups (FDR < 0.1) in BALF and lung tissue homogenates, respectively. Of those, HGF, TGF-α, and CCL2 were identified as the most relevant to this study. Their protein expression patterns were verified by ELISA . This study confirmed that post- stroke lung damage was not associated with increased lung permeability or cerebral ischemia severity. Furthermore, the dysregulation of HGF, TGF-α, and CCL2 in BALF and lung tissue after ischemia could play an important role in the molecular mechanisms underlying stroke -induced lung damage.