title: Interaction between allergic asthma and atherosclerosis.
abstract: Prior studies have established an essential role of mast cells in allergic asthma and atherosclerosis. Mast cell deficiency or inactivation protects mice from allergen-induced airway hyper-responsiveness and diet-induced atherosclerosis, suggesting that mast cells share pathologic activities in both diseases. Allergic asthma and atherosclerosis are inflammatory diseases that contain similar sets of elevated numbers of inflammatory cells in addition to mast cells in the airway and arterial wall, such as macrophages, monocytes, T cells, eosinophils, and smooth muscle cells. Emerging evidence from experimental models and human studies points to a potential interaction between the 2 seemingly unrelated diseases. Patients or mice with allergic asthma have a high risk of developing atherosclerosis or vice versa, despite the fact that asthma is a T-helper (Th)2-oriented disease, whereas Th1 immunity promotes atherosclerosis. In addition to the preferred Th1/Th2 responses that may differentiate the 2 diseases, mast cells and many other inflammatory cells also contribute to their pathogenesis by more than just T cell immunity. Here, we summarize the different roles of airway and arterial wall inflammatory cells and vascular cells in asthma and atherosclerosis and propose an interaction between the 2 diseases, although limited investigations are available to delineate the molecular and cellular mechanisms by which 1 disease increases the risk of the other. Results from mouse allergic asthma and atherosclerosis models and from human population studies lead to the hypothesis that patients with atherosclerosis may benefit from antiasthmatic medications or that the therapeutic regimens targeting atherosclerosis may also alleviate allergic asthma.
authors.affiliation: Department of Cardiology, Institute of Clinical Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China; Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Mass.
authors.forename: Cong-Lin
authors.initials: CL
authors.lastname: Liu
authors.affiliation: Department of Cardiology, Institute of Clinical Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
authors.forename: Jin-Ying
authors.initials: JY
authors.lastname: Zhang
authors.affiliation: Department of Cardiology, Institute of Clinical Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China; Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Mass. Electronic address: gshi@rics.bwh.harvard.edu.
authors.forename: Guo-Ping
authors.initials: GP
authors.lastname: Shi
mesh_terms: D001249:Asthma / Q000150:complications* / Q000276:immunology; D050197:Atherosclerosis / Q000150:complications* / Q000453:epidemiology / Q000276:immunology; D006801:Humans; D006967:Hypersensitivity / Q000150:complications*; D007962:Leukocytes / Q000473:pathology; D015289:Leukotrienes / Q000378:metabolism; D050356:Lipid Metabolism
chemical_list: D015289:Leukotrienes