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.
Abbreviations:
BAL (bronchoalveolar lavage), LDL (low-density lipoprotein), SMC (smooth muscle cell), TNF- (tumor necrosis factor-), LDLr (LDL receptor), Apoe (apolipoprotein E), OVA (ovalbumin), IMT (intima-media thickness), SMCs (smooth muscle cells), CI (confidence interval), OR (odds ratio), SUVmax (maximum standardized uptake value), MHC-I (major histocompatibility complex class-I), CHD (coronary heart disease), HDM (House dust mite), mMCP-6 (Mouse mast cell protease-6), MCP-1 (monocyte chemoattractant protein-1), PLA2 (phospholipase A2), COX-2 (cyclooxygenase-2), NF-B (nuclear factor-B), AP-1 (activator protein-1), RANTES (regulated on activation, normal T cell expressed and secreted), CCR2/CCL2 (chemokine (C-C Motif) Receptor 2/chemokine (C-C motif) ligand 2), PECAM-1 (platelet endothelial cell adhesion molecule-1), MCP-1 (monocyte chemoattractant protein-1), DRA (dust mite (Dermatophagoides farinae), ragweed, and Aspergillus sp.), LPS (lipopolysaccharide), GSK (glycogen synthase kinase), STAT-3 (signal transducer and Activator of transcription-3), CXCL4 (CXC chemokine ligand 4), ACT (asthma control test), SNPs (single nucleotide polymorphisms), GATA3 (GATA binding protein 3), Treg (regulatory T cell), CADs (coronary artery diseases), miRs (MicroRNAs), NOR-1 (neuronderived orphan receptor-1), 5-LO (5-lipoxygenase), LTA4 (leukotriene A4), GM-CSF (granulocyte-macrophage colony-stimulating factor), FLAP (5-LO–activating protein), HDL-C (high-density lipoprotein cholesterol), VLDL (very low-density lipoprotein)To read this article in full you will need to make a payment
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Article info
Publication history
Published online: October 06, 2015
Accepted:
September 29,
2015
Received in revised form:
September 25,
2015
Received:
August 2,
2015
Identification
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© 2015 Elsevier Inc. All rights reserved.
