Our understanding of vascular pathology relies on inducible animal models of disease that remain poorly described, and concern exists regarding indirect effects of the inducing agents. We sought to perform a detailed characterization of the immune response to a commonly used murine aneurysm model. Aneurysms were generated in 10 adult C57/Bl6 mice using 2 weeks of oral beta-amino propriono-nitrile (BAPN) administration and 4 weeks of angiotensin-2 (AT2) delivered via osmotic pump. FACS analysis was used to characterize progenitor and hematopoietic cell lines in bone marrow, blood and aorta. 3 mice died of aortic rupture between days 8 and 9. The remaining 7 were compared to age-matched controls. BAPN/AT2 treatment caused aortic dilatation at all aortic regions from the root to the descending thoracic aorta (P<0.01). The suprarenal aorta was aneurysmal in all BAPN/AT2 mice with a maximum diameter of 1.86±0.1mm compared to controls 0.98±0.03mm (P<0.001). In the blood, total cells counts at day 2, 16 and 28 were increased (P<0.001). CD45-2 and B-cell counts were significantly increased in the BAPN/AT2 mice compared to controls (P<0.001). The aorta of BAPN/AT2 mice had significantly increased macrophage counts (P<0.001) with no difference in monocytes, neutrophils, T or B cell counts. Aortic tissue macrophages were predominantly G0 G1 (97±1%) phase. The bone marrow CD45-2 compartment was similar in aneurysmal BAPN/AT2 and control mice but Ly6C lo-inter monocytes were increased in BAPN/AT2 mice. Marrow CD117+/lin- hematopoietic progenitor and stem cells (P=0.4), and differential counts of CD117+/Sca1+ hematopoietic stem cells and CD117+/Sca1- progenitor cells were similar in control and BAPN/AT2 treated mice. BAPN/AT2 induces aortic disease with aneurysmal degeneration of the suprarenal aorta. We observed a significant decrease in aortic macrophage proliferation suggestive of a mechanism of expansion independent of local macrophage proliferation. We did not observe a significant change in the bone marrow stem or progenitor cell compartment suggesting aortic injury is driving inflammation rather than direct stimulus of the marrow compartment by BAPN/AT2.