Role of the neutrophil in abdominal aortic aneurysm development

Elastase release by neutrophils has been implicated in the etiology of abdominal aortic aneurysm (AAA). The present study investigated whether neutrophils in patients with AAA actively synthesize the neutrophil elastase enzyme and the effect of elastin-derived peptides on neutrophil elastase release. Total neutrophil elastase in patients with AAA was significantly higher than in those with aortic occlusive disease and controls. The neutrophil elastase gene was not expressed in any patient group. Elastin-derived peptides induced elastase release, which was significantly higher in patients with AAA than in those with aortic occlusive disease and controls. These data indicate that the peptides of elastin degradation stimulate the release of elastase, but that continuing production of elastase is absent in circulating neutrophils. It is concluded that: (1) neutrophils do not actively synthesize elastase but act as 'mules' or carriers of the enzyme; and (2) elastin breakdown products stimulate the release of elastase at the aortic wall by circulating neutrophils, which in patients with AAA have a predetermined increased amount of elastase.