Abstract
Acute rejection after lung transplantation is the main risk factor for the development of bronchiolitis obliterans syndrome (BOS). Carbon monoxide (CO) can provide beneficial antiapoptotic and anti-inflammatory effects in the context of ischemia–reperfusion injury (IRI), and may serve to limit tissue inflammation and injury in the setting of airway transplant rejection. Here we tested the ability of carbon monoxide releasing molecules (CORMs) to prevent airway rejection in established mouse orthotopic and heterotopic trachea transplant models.
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