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Basic science: Cardiovascular disease basic research
e0118 The myeloperoxidase inhibitor, aminobenzoic acid hydrazide, alters neutrophil-endothelial cell interaction
  1. Han Lili,
  2. Shen Xiaoli,
  3. Lin Saimei,
  4. Pan Leng,
  5. Liu Xiaoqing,
  6. Pu Xiaodong,
  7. Deng Yulian,
  8. Guo Conghua
  1. Affiliated Fujian Provincial Hospital, Fujian Medical University/Fujian Provincial Key Laboratory of Cardiovascular Disease

Abstract

Objective Acute myocardial infarctions (AMI) are associated with vascular inflammation, including activation of neutrophils and their adherence to vascular endothelial cells via CD11b/CD18 binding to intercellular adhesion molecule (ICAM). Myeloperoxidase (MPO) is an inflammatory biomarker, can induce CD11b surface expression in polymorphonuclear neutrophils (PMNs), but its role in regulating adhesion is not well characterised. MPO's role in regulating adhesion was further investigated by comparing the effects of aminobenzoic acid hydrazide (ABAH), an inhibitor of MPO, antibodies specific for CD11b and vehicle control on PMN adhesion to endothelial cells.

Methods Human neutrophils were isolated from the peripheral blood of patients with AMI or healthy participants using Percoll density gradient centrifugation. The effects of ABAH and anti-CD11b antibodies on neutrophil adhesion to endothelial cell were measured using adhesion assays.

Results The adhesion rate was significantly higher for neutrophils isolated from AMI patients than healthy individuals (p<0.001). Neutrophil adhesion was reduced upon treatment with ABAH in a dose dependent manner. The adhesion rate was significantly reduced in neutrophils treated with 10 μM and 20 μM ABAH as compared to the untreated group. Treatment with anti-CD11b antibodies also significantly reduced neutrophil adhesion compared to the untreated control group (p<0.001).

Conclusions MPO might enhance the neutrophils adhesions to endothelial cells in AMI patients through the upregulation of CD11b expression in the suface of neutrophils. The interference of cell adhesion by ABAH may be mediated by reduced CD11b expression in neutrophils.

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