Abstract 104: EBI3 Deficiency Exacerbates Experimental Abdominal Aortic Aneurysms
Background: Abdominal aortic aneurysms (AAAs) are an age-and gender-related chronic vascular disease. Ebi3 (EB virus-induced gene 3) encodes a cytokine subunit protein shared by two anti-inflammatory cytokines IL-27 and IL-35. Given the importance of inflammation in AAA pathogenesis, we evaluated the influence of Ebi3 deficiency on experimental AAAs.
Methods and Results: AAAs were created in10 week old male Ebi3-knoctout (KO) and wild type (WT) mice via the intra-aortic infusion of porcine pancreatic elastase (PPE), and evaluated using in vivo transabdominal ultrasonography and histology at sacrifice (Figure). Following PPE infusion, KO mice experienced more significant and rapid aneurysmal aortic enlargement. All KO and WT mice developed AAAs (≥50% diameter increase) within 7 and 14 days, respectively. Medial elastin and smooth muscle cell attenuation were more pronounced in aneurysmal aortae of KO mice, as were both aortic macrophage and T cell infiltration. However, no difference in aortic B cell infiltration or mural angiogenesis was noted between groups.
Conclusions: Ebi3 deficiency promotes the onsets and progression of experimental AAAs in association with increased aortic accumulation of macrophages and T cells. Our study suggests a protective role of Ebi3 in experimental AAAs, potentially related to IL-27 and/or IL-35 production.
Author Disclosures: Y. Iida: None. H. Tanaka: None. X. Hu: None. X. Xiong: None. H. Zhao: None. B. Xu: None. R.L. Dalman: None.
- © 2014 by American Heart Association, Inc.