
This study aimed to investigate mechanisms of increased neutrophil adhesion in AATD and whether alpha-1 antitrypsin (AAT) augmentation therapy abrogates this effect. The effect of once-weekly intravenous AAT augmentation therapy was assessed by calcium fluorometric, μ-calpain, and cell adhesion assays. Treatment of AAT-deficient individuals with AAT augmentation therapy resulted in increased caveolin-1 and membrane cholesterol content, with concurrent decreased neutrophil integrin expression and adhesion. In addition, results demonstrate an additional benefit of AAT augmentation therapy, evidenced by decreased circulating inflammation and controlled neutrophil adhesion.
Like
Save
Share