FIG. 3.

Different origins and modes of action of tissue macrophages in AAA. Myelopoiesis in the bone marrow is the source of circulating blood monocytes with the spleen acting as a reservoir. Extravasation of “passenger” monocytes into the aneurysm wall is a CD14-dependent mechanism. In parallel, a pool of “resident” tissue macrophages exists, which originate from the yolk sac and migrate into aortic tissue during embryonic development. During the early phase of AAA development, a shift toward M1 macrophages entails increased secretion of proinflammatory cytokines, including TNF-α, IL-6, IL-1β, iNOS, MCP-1, and ECM degrading products such as MMP-9. The inflammatory response within the aneurysm wall is a self-perpetuating system, as degradation products act as chemokines to attract further monocytes to extravasate. CMP, common myeloid progenitor; ECM, extracellular matrix; HSC, hematopoietic stem cell; MMP, matrix metalloproteinase; TNF-α, tumor necrosis factor alpha. Color images are available online.