Abstract | OBJECTIVE: 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.
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Authors | Cong-Lin Liu, Yi Wang, Mengyang Liao, Holger Wemmelund, Jingyuan Ren, Cleverson Fernandes, Yi Zhou, Galina K Sukhova, Jes S Lindholt, Søren P Johnsen, Jin-Ying Zhang, Xiang Cheng, Xiaozhu Huang, Alan Daugherty, Bruce D Levy, Peter Libby, Guo-Ping Shi |
Journal | Arteriosclerosis, thrombosis, and vascular biology
(Arterioscler Thromb Vasc Biol)
Vol. 36
Issue 1
Pg. 69-77
(Jan 2016)
ISSN: 1524-4636 [Electronic] United States |
PMID | 26543094
(Publication Type: Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't)
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Copyright | © 2015 American Heart Association, Inc. |
Chemical References |
- Anti-Allergic Agents
- Antibodies, Monoclonal
- Apolipoproteins E
- Inflammation Mediators
- Angiotensin II
- Immunoglobulin E
- Ovalbumin
- Calcium Chloride
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Topics |
- Angiotensin II
- Animals
- Anti-Allergic Agents
(pharmacology)
- Antibodies, Monoclonal
(pharmacology)
- Aorta, Abdominal
(drug effects, immunology, metabolism, pathology)
- Aortic Aneurysm, Abdominal
(chemically induced, immunology, metabolism, pathology, prevention & control)
- Apolipoproteins E
(deficiency, genetics)
- Calcium Chloride
- Dilatation, Pathologic
- Disease Models, Animal
- Disease Progression
- Immunoglobulin E
(blood, immunology)
- Inflammation Mediators
(immunology, metabolism)
- Lung
(immunology, metabolism)
- Macrophages
(immunology, metabolism)
- Male
- Mast Cells
(immunology, metabolism)
- Mice, Inbred C57BL
- Mice, Knockout
- Ovalbumin
- Pneumonia
(chemically induced, complications, immunology, metabolism, prevention & control)
- Respiratory Hypersensitivity
(chemically induced, complications, immunology, metabolism, prevention & control)
- Risk Factors
- Signal Transduction
- Vascular Remodeling
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