In the angiotensin II-induced abdominal aortic aneurysm (AAA) mouse model, AngII enhances TREM-1 production via AngII receptors, which affects monocyte mobilization from the spleen and infiltration into the aortic wall. Consequently, TREM-1 activation promotes monocyte penetration into the aorta and triggers a proinflammatory response, exacerbating AAA severity. Trem1−/− (Apoe−/−Trem1−/−) mice exhibited reduced AAA progression and severity by decreasing aortic inflammation and lowering the expression of Il1b, Tnfa, Mmp2, and Mmp9 mRNA, along with reducing macrophage content. Here, MMP2 is linked to triple-A syndrome.