Macrophage Phenotypes In Murine Aneurysm

A prominent pathological feature of abdominal aortic aneurysm (AAA) is the infiltration of mononuclear phagocytes such as macrophages. Accumulating literature has highlighted the importance of macrophage phenotypes and their role in vascular disease. Inflammatory (M1) macrophages produce proteases and proinflammatory cytokines, while alternatively activated (M2) macrophages produce anti‐inflammatory cytokines and extracellular matrix (ECM) components. Using an elastase‐induced model of murine AAA, we tested the hypothesis that aneurysm induction shifts M1/M2 balance toward inflammation. Leukocytes were isolated from the aortic tissue and analyzed by flow cytometry. Three days after surgery, arteries treated with elastase (aneurysm) or inactivated elastase (control) contained similar levels of total macrophages (7aad‐CD45+CD11b+F4/80+). However, as disease progressed, aneurysmal aorta displayed significantly higher number of macrophages than controls ~2.15 and 1.28 fold higher 7 and 14 days after surgery, respectively. Interestingly, the M1:M2 ratio (CD86+:CD206+) was higher in aneurysm arteries, largely due to a selective suppression of M2 polarization. These data suggest an imbalance between M1 and M2 macrophages may contribute to a chronic inflammatory state during aneurysm progression. Funding provided by NRSA T32 HL 07936 from the NHLBI.