Cong-Lin Liu1, Yi Wang1, Mengyang Liao1, Holger Wemmelund1, Jingyuan Ren1, Cleverson Fernandes1, Yi Zhou1, Galina K Sukhova1, Jes S Lindholt1, Søren P Johnsen1, Jin-Ying Zhang1, Xiang Cheng1, Xiaozhu Huang1, Alan Daugherty1, Bruce D Levy1, Peter Libby1, Guo-Ping Shi2. 1. From the Department of Cardiology, Institute of Clinical Medicine, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, China (C.-L.L., J.-Y.Z., G.-P.S.); Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA (C.-L.L., Y.W., M.L., J.R., C.F., Y.Z., G.K.S., B.D.L., P.L., G.-P.S.); Department of Cardiology, Shanghai First People's Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China (Y.W.); Laboratory of Cardiovascular Immunology, Institute of Cardiology, Union Hospital, Tongji Medical College of Huazhong University of Science and Technology, Wuhan, China (M.L., X.C.); Department of Vascular Surgery, Viborg Regional Hospital, Viborg, Denmark (H.W.); Department of Hypertension, Beijing Anzhen Hospital, Capital Medical University, Beijing, China (J.R.); Department of Clinical Epidemiology, Institute of Clinical Medicine, Aarhus University Hospital, Aarhus, Denmark (H.W., S.P.J.); Department of Cardiothoracic and Vascular Surgery, Elitary Research Centre of Individualized Medicine of Arterial Disease, Odense University Hospital, Odense, Denmark (J.S.L.); Department of Medicine, University of California, San Francisco (X.H.); and Saha Cardiovascular Research Center, University of Kentucky, Lexington (A.D.). 2. From the Department of Cardiology, Institute of Clinical Medicine, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, China (C.-L.L., J.-Y.Z., G.-P.S.); Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA (C.-L.L., Y.W., M.L., J.R., C.F., Y.Z., G.K.S., B.D.L., P.L., G.-P.S.); Department of Cardiology, Shanghai First People's Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China (Y.W.); Laboratory of Cardiovascular Immunology, Institute of Cardiology, Union Hospital, Tongji Medical College of Huazhong University of Science and Technology, Wuhan, China (M.L., X.C.); Department of Vascular Surgery, Viborg Regional Hospital, Viborg, Denmark (H.W.); Department of Hypertension, Beijing Anzhen Hospital, Capital Medical University, Beijing, China (J.R.); Department of Clinical Epidemiology, Institute of Clinical Medicine, Aarhus University Hospital, Aarhus, Denmark (H.W., S.P.J.); Department of Cardiothoracic and Vascular Surgery, Elitary Research Centre of Individualized Medicine of Arterial Disease, Odense University Hospital, Odense, Denmark (J.S.L.); Department of Medicine, University of California, San Francisco (X.H.); and Saha Cardiovascular Research Center, University of Kentucky, Lexington (A.D.). gshi@rics.bwh.harvard.edu.
Abstract
OBJECTIVE: Asthma and abdominal aortic aneurysms (AAA) both involve inflammation. Patients with asthma have an increased risk of developing AAA or experiencing aortic rupture. This study tests the development of one disease on the progression of the other. APPROACH AND RESULTS: Ovalbumin sensitization and challenge in mice led to the development of allergic lung inflammation (ALI). Subcutaneous infusion of angiotensin II into mice produced AAA. Simultaneous production of ALI in AAA mice doubled abdominal aortic diameter and increased macrophage and mast cell content, arterial media smooth muscle cell loss, cell proliferation, and angiogenesis in AAA lesions. ALI also increased plasma IgE, reduced plasma interleukin-5, and increased bronchioalveolar total inflammatory cell and eosinophil accumulation. Intraperitoneal administration of an anti-IgE antibody suppressed AAA lesion formation and reduced lesion inflammation, plasma IgE, and bronchioalveolar inflammation. Pre-establishment of ALI also increased AAA lesion size, lesion accumulation of macrophages and mast cells, media smooth muscle cell loss, and plasma IgE, reduced plasma interleukin-5, interleukin-13, and transforming growth factor-β, and increased bronchioalveolar inflammation. Consequent production of ALI also doubled lesion size of pre-established AAA and increased lesion mast cell and T-cell accumulation, media smooth muscle cell loss, lesion cell proliferation and apoptosis, plasma IgE, and bronchioalveolar inflammation. In periaortic CaCl2 injury-induced AAA in mice, production of ALI also increased AAA formation, lesion inflammation, plasma IgE, and bronchioalveolar inflammatory cell accumulation. CONCLUSIONS: This study suggests a pathological link between airway allergic disease and AAA. Production of one disease aggravates the progression of the other.
OBJECTIVE:Asthma and abdominal aortic aneurysms (AAA) both involve inflammation. Patients with asthma have an increased risk of developing AAA or experiencing aortic rupture. This study tests the development of one disease on the progression of the other. APPROACH AND RESULTS:Ovalbumin sensitization and challenge in mice led to the development of allergic lung inflammation (ALI). Subcutaneous infusion of angiotensin II into mice produced AAA. Simultaneous production of ALI in AAAmice doubled abdominal aortic diameter and increased macrophage and mast cell content, arterial media smooth muscle cell loss, cell proliferation, and angiogenesis in AAA lesions. ALI also increased plasma IgE, reduced plasma interleukin-5, and increased bronchioalveolar total inflammatory cell and eosinophil accumulation. Intraperitoneal administration of an anti-IgE antibody suppressed AAA lesion formation and reduced lesion inflammation, plasma IgE, and bronchioalveolar inflammation. Pre-establishment of ALI also increased AAA lesion size, lesion accumulation of macrophages and mast cells, media smooth muscle cell loss, and plasma IgE, reduced plasma interleukin-5, interleukin-13, and transforming growth factor-β, and increased bronchioalveolar inflammation. Consequent production of ALI also doubled lesion size of pre-established AAA and increased lesion mast cell and T-cell accumulation, media smooth muscle cell loss, lesion cell proliferation and apoptosis, plasma IgE, and bronchioalveolar inflammation. In periaortic CaCl2 injury-induced AAA in mice, production of ALI also increased AAA formation, lesion inflammation, plasma IgE, and bronchioalveolar inflammatory cell accumulation. CONCLUSIONS: This study suggests a pathological link between airway allergic disease and AAA. Production of one disease aggravates the progression of the other.
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