%0 Journal Article
%T IL-33 in murine abdominal aortic aneurysm: a novel inflammatory mediator awaiting clinical translation
%A Shirling Tsai
%A Xunde Xian
%J SCIE-indexed Journal
%D 2019
%R 10.21037/jtd.2019.06.20
%X Abdominal aortic aneurysm (AAA) affects approximately 5% of the high-risk general population consisting of men between the ages of 60¨C75 (1). Histopathologically, AAA are characterized by degradation of the extracellular matrix (particularly elastin), medial smooth muscle cell (SMC) depletion or apoptosis, and inflammation (2,3). Very little is known about risk factors for AAA expansion, once an aneurysm has been detected. Increasing aneurysm size and smoking have been associated with faster aneurysm growth, while diabetes has been associated with slower growth (4). The role of inflammation in AAA has been tested and explored for decades. Studies of human AAA have demonstrated the presence of inflammatory cells in all layers of the aortic aneurysm wall as well as in the associated mural thrombus (5). Understanding the function of these inflammatory cells has been the focus for many research groups. Baxter¡¯s group has proposed that AAA formation and progression is associated with an imbalance in M1/M2 macrophage polarization, resulting in a preponderance of pro-inflammatory M1 macrophages and relative deficiency of anti-inflammatory M2 macrophages (6,7). Others have demonstrated that AAA are associated with a deficiency of regulatory T cells (Treg) (8,9). The chronic inflammatory state is further supported by the presence of circulating pro-inflammatory cytokines, such as IL-6, IL-1¦Â, tumor necrosis factor-¦Á (TNF-¦Á) and interferon-gamma (IFN-¦Ã) in patients with AAA (10). In animal models of AAA, inhibition of IL-1¦Â (6) and TNF-¦Á (11) have been associated with protection from AAA formation, decreased macrophage infiltration, and preservation of elastin layers
%U http://jtd.amegroups.com/article/view/29460/html