Abstract
BackgroundTreatment of acute lung injury (ALI) remains an unsolved problem in intensive care medicine. Recruitment of neutrophils into the lungs, regarded as a key mechanism in progression of ALI, depends on signaling between neutrophils and platelets. Consequently we explored the effect of platelet-targeted aspirin and tirofiban treatment in endotoxin induced acute lung injuryMethodsC57Bl/6 mice were exposed to aerosolized LPS (500μg/ml) for 30min and treated with Aspirin (100μg/g bodyweight via intraperitoneal injection, 30 min before or 1 hour after LPS inhalation) or Tirofiban (0.5μg/ g bodyweight via tail vein injection 30 min before or 1 hour after LPS inhalation). The count of alveolar, interstitial, and intravascular neutrophils was assessed 4h later by flow cytometry. Lung permeability changes were assessed by FITC-dextran clearance and protein content in the BAL fluid.ResultsAspirin both before and after LPS inhalation reduced neutrophil influx into the lung and lung permeability indicating the protective role of Aspirin in ALI. Tirofiban, however, did not alter neutrophil recruitment after LPS inhalation. Release of platelet-derived chemokines CCL5 and PF4 and neutrophil extracellular traps was reduced by Aspirin but not by Tirofiban.ConclusionAspirin, but not Tirofiban reduces neutrophil recruitment and displays protective effects during endotoxin induced lung injury.
Highlights
Considerable progress has been made in understanding pathophysiology of acute lung injury (ALI) and despite all innovations in intensive care medicine, the mortality of ALI remains up to 40% with an age-adjusted incidence of 86.2 per 100.000 person-years [1]
Aspirin both before and after LPS inhalation reduced neutrophil influx into the lung and lung permeability indicating the protective role of Aspirin in ALI
Release of platelet-derived chemokines CCL5 and PF4 and neutrophil extracellular traps was reduced by Aspirin but not by Tirofiban
Summary
Considerable progress has been made in understanding pathophysiology of acute lung injury (ALI) and despite all innovations in intensive care medicine, the mortality of ALI remains up to 40% with an age-adjusted incidence of 86.2 per 100.000 person-years [1]. ALI and ARDS are characterized by an increased permeability of the alveolar-capillary barrier resulting in lung edema with protein-rich fluid, resulting in impairment of arterial oxygenation. Treatment of acute lung injury (ALI) remains an unsolved problem in intensive care medicine. Recruitment of neutrophils into the lungs, regarded as a key mechanism in progression of ALI, depends on signaling between neutrophils and platelets. We explored the effect of platelet-targeted aspirin and tirofiban treatment in endotoxin induced acute lung injury
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