ArticleAmerican journal of physiology. Lung cellular and molecular physiology2012
Human apolipoprotein E genotypes differentially modify house dust mite-induced airway disease in mice.
Article in American journal of physiology. Lung cellular and molecular physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 14 citations in OpenAlex.
- Interactions Between HDL and CD4+ T Cells: A Novel Understanding of HDL Anti-Inflammatory Properties.Arteriosclerosis, thrombosis, and vascular biology · 2024Review
- Plasma proteomics reveals gestational age-specific responses to mechanical ventilation and identifies the mechanistic pathways that initiate preterm lung injury.Scientific reports · 2018Article
- A New Frontier in Immunometabolism. Cholesterol in Lung Health and Disease.Annals of the American Thoracic Society · 2017Review
- Protective role of the apolipoprotein E2 allele in age-related disease traits and survival: evidence from the Long Life Family Study.Biogerontology · 2016Article
- Emerging Roles of Apolipoprotein E and Apolipoprotein A-I in the Pathogenesis and Treatment of Lung Disease.American journal of respiratory cell and molecular biology · 2016Review
- Secretoglobin Superfamily Protein SCGB3A2 Alleviates House Dust Mite-Induced Allergic Airway Inflammation in Mice.International archives of allergy and immunology · 2016Article
- Obesity shifts house dust mite-induced airway cellular infiltration from eosinophils to macrophages: effects of glucocorticoid treatment.Immunologic research · 2015Article
- Regulation of Adaptive Immunity in Health and Disease by Cholesterol Metabolism.Current allergy and asthma reports · 2015Review
- Gata5 deficiency causes airway constrictor hyperresponsiveness in mice.American journal of respiratory cell and molecular biology · 2014Article
- Cholesterol selectively regulates IL-5 induced mitogen activated protein kinase signaling in human eosinophils.PloS one · 2014Article
- Apolipoprotein A-I attenuates ovalbumin-induced neutrophilic airway inflammation via a granulocyte colony-stimulating factor-dependent mechanism.American journal of respiratory cell and molecular biology · 2012Article
Corrections and comments
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Authors and funding
19 authors at 6 institutions in 3 countries.
Funding
Abstract
Apolipoprotein E (apoE) is an endogenous negative regulator of airway hyperreactivity (AHR) and mucous cell metaplasia in experimental models of house dust mite (HDM)-induced airway disease. The gene encoding human apoE is polymorphic, with three common alleles (ε2, ε3, and ε4) reflecting single amino acid substitutions at amino acids 112 and 158. The objective of this study was to assess whether the human apoE alleles modify airway responses to repeated nasal HDM challenges. Mice expressing the human apoE ε2 (huApoE2), ε3 (huApoE3), or ε4 (huApoE4) alleles received nasal HDM challenges, and airway responses were compared with mice expressing the endogenous murine apoE gene (muApoE). huApoE3 mice displayed significant reductions in AHR, mucous cell metaplasia, and airway inflammation compared with muApoE mice. The attenuated severity of airway inflammation in huApoE3 mice was associated with reductions in lung mRNA levels of Th2 and Th17 cytokines, as well as chemokines (CCL7, CCL11, CCL24). huApoE4 mice had an intermediate phenotype, with attenuated AHR and IgE production, compared with muApoE mice, whereas airway inflammation and mucous cell metaplasia were not reduced. In contrast, HDM-induced airway responses were not modified in mice expressing the huApoE2 allele. We conclude that the polymorphic huApoE alleles differentially modulate HDM-induced airway disease, which can be stratified, in rank order of increasing disease severity, ε3 < ε4 < ε2. These results raise the possibility that the polymorphic apoE alleles may modify disease severity in human asthma.
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