Aminobenzoic acid hydrazide, a myeloperoxidase inhibitor, alters the adhesive properties of neutrophils isolated from acute myocardial infarction patients

Acute myocardial infarction (AMI) is associated with vascular inflammation, including activation and adherence of neutrophils to vascular endothelial cells via CD11b/CD18 intercellular adhesion molecule interactions. Myeloperoxidase (MPO) induces CD11b surface expression in polymorphonuclear neutrophils (PMNs); however, its role in regulating adhesion in AMI is not well characterized. This study investigates the effects of aminobenzoic acid hydrazide (ABAH), an inhibitor of MPO, antibodies specific for CD11b, on the adhesion of PMNs isolated from AMI patients to endothelial cells. Human neutrophils were isolated from the peripheral blood of 20 patients with AMI or 20 healthy participants as control using Percoll density gradient centrifugation. The major biochemical indicators were detected with different biochemical analyses. The effects of ABAH and anti-CD11b antibodies on neutrophil adhesion to endothelial cell were measured using adhesion assays in vitro. The adhesion rate was significantly higher for neutrophils isolated from AMI patients than healthy individuals (P < 0.001). ABAH significantly inhibited MPO activity in PMNs isolated from AMI patients. Neutrophil adhesion was significantly reduced upon treatment with 10 and 20 μM ABAH in a dose-dependent manner. Treatment with anti-CD11b antibodies also significantly reduced neutrophil adhesion in comparison with the untreated control group (P < 0.001). Thus, both ABAH and anti-CD11b antibodies reduced PMN adhesion. Further studies are necessary to determine whether MPO enhances neutrophil adhesion to endothelial cells in AMI patients through the upregulation of CD11b expression on the surface of neutrophils, which is abrogated by ABAH.