Get 20M+ Full-Text Papers For Less Than $1.50/day. Start a 14-Day Trial for You or Your Team.

Learn More →

Role of epigenetics and DNA-damage in asthma

Role of epigenetics and DNA-damage in asthma Purpose of reviewAlthough asthma is a common disease worldwide, its pathogenesis remains to be fully elucidated. There is increasing evidence of the interaction between epigenetics, DNA-damage, and environmental allergens in the development of asthma. In this review, we will focus on the role of epigenetics and DNA-damage in asthma.Recent findingsThere is growing evidence of environmental allergens, particularly house dust mite, stimulating oxidative DNA damage in airway epithelial cells. The repair of this DNA damage has been implicated in the secretion of Th2 cytokines and the induction of allergic inflammation.SummaryStudies of the role of epigenetics, DNA-damage, and environmental allergens have begun to reveal the their complex interactions and their roles in the development of asthma. Further study in these areas may lead to novel prevention and treatment approaches. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Current Opinion in Allergy and Clinical Immunology Wolters Kluwer Health

Role of epigenetics and DNA-damage in asthma

Download PDF
6 pages

Loading next page...
 
/lp/wolters-kluwer-health/role-of-epigenetics-and-dna-damage-in-asthma-0s0E9LoVqv

References

References for this paper are not available at this time. We will be adding them shortly, thank you for your patience.

Publisher
Wolters Kluwer Health
Copyright
Copyright © 2018 Wolters Kluwer Health, Inc. All rights reserved.
ISSN
1528-4050
eISSN
1473-6322
DOI
10.1097/ACI.0000000000000415
pmid
29189349
Publisher site
See Article on Publisher Site

Abstract

Purpose of reviewAlthough asthma is a common disease worldwide, its pathogenesis remains to be fully elucidated. There is increasing evidence of the interaction between epigenetics, DNA-damage, and environmental allergens in the development of asthma. In this review, we will focus on the role of epigenetics and DNA-damage in asthma.Recent findingsThere is growing evidence of environmental allergens, particularly house dust mite, stimulating oxidative DNA damage in airway epithelial cells. The repair of this DNA damage has been implicated in the secretion of Th2 cytokines and the induction of allergic inflammation.SummaryStudies of the role of epigenetics, DNA-damage, and environmental allergens have begun to reveal the their complex interactions and their roles in the development of asthma. Further study in these areas may lead to novel prevention and treatment approaches.

Journal

Current Opinion in Allergy and Clinical Immunology – Wolters Kluwer Health

Published: Feb 1, 2018

References

  • The environment, epigenome, and asthma
  • IgE and eosinophils as therapeutic targets in asthma
  • Recent advances in the epigenetics and genomics of asthma
  • Finding the missing heritability of complex diseases
  • Epigenetic mechanisms in asthma
  • Redox control of asthma: molecular mechanisms and therapeutic opportunities
  • Nitrative stress in inflammatory lung diseases
  • Increase in the heritability of asthma from 1994 to 2003 among adolescent twins
  • A comparison of genetic and environmental variance structures for asthma, hay fever and eczema with symptoms of the same diseases: a study of Norwegian twins
  • Interleukin-1R antagonist gene and prenatal smoke exposure are associated with childhood asthma
  • Prenatal exposure to a farm environment modifies atopic sensitization at birth
  • Farm exposure in utero may protect against asthma, hay fever and eczema
  • Gender differences in asthma
  • Parental history and the risk for childhood asthma. Does mother confer more risk than father?
  • Maternal inheritance of atopic IgE responsiveness on chromosome 11q
  • Parental and neonatal risk factors for atopy, airway hyper-responsiveness, and asthma
  • Synthesis of T helper 2-type cytokines at the maternal-fetal interface
  • Fine mapping and positional candidate studies identify HLA-G as an asthma susceptibility gene on chromosome 6p21
  • A polymorphism∗ in the 5’ flanking region of the CD14 gene is associated with circulating soluble CD14 levels and with total serum immunoglobulin E
  • Pro: genome-wide association studies (GWAS) in asthma
  • Asthma genetics 2006: the long and winding road to gene discovery
  • Applying epidemiologic concepts of primary, secondary, and tertiary prevention to the elimination of racial disparities in asthma
  • Reported asthma among Puerto Rican, Mexican-American, and Cuban children, 1982 through 1984
  • Asthma mortality in U.S. Hispanics of Mexican, Puerto Rican, and Cuban Heritage, 1990-1995
  • Epigenetics, asthma, and allergic diseases: a review of the latest advancements
  • DNA methylation patterns and epigenetic memory
  • Phenotypic plasticity and the epigenetics of human disease
  • The history of cancer epigenetics
  • Human DNA methylomes at base resolution show widespread epigenomic differences
  • Human body epigenome maps reveal noncanonical DNA methylation variation
  • Uncovering the role of 5-hydroxymethylctyosine in the epigenome
  • Genomic DNA methylation: the mark and its mediators
  • Mammalian DNA methyltransferases: a structural perspective
  • Epigenetics in asthma and allergy
  • Blood and nasal epigenetics correlate with allergic rhinitis symptom development in the environmental exposure unit
  • Dissecting childhood asthma with nasal transcriptomics distinguishes subphenotypes of disease
  • The nasal methylome and childhood atopic asthma
  • Genome-wide interaction study of dust mite allergen on lung function in children with asthma
  • Histone methylation: a dynamic mark in health, disease and inheritance
  • Charting histone modifications and functional organization of mammalian genomes
  • Variants of DENND1B associated with asthma in children
  • Perinatal nicotine exposure induces asthma in second generation offspring
  • Aeroallergens induce reactive oxygen species production and DNA damage and dampen antioxidant responses in bronchial epithelial cells
  • Maternal phthalate exposure promotes allergic airway inflammation over 2 generations through epigenetic modifications
  • Epigenome-wide analysis links SMAD3 methylation at birth to asthma in children of asthmatic mothers
  • Antimalarial drug artesunate ameliorates oxidative lung damage in experimental allergic asthma
  • ROS generated by pollen NADPH oxidase provide a signal that augments antigen induced allergic airway inflammation
  • House dust mite-induced asthma causes oxidative damage and DNA double-strand breaks in the lung
  • Homologous recombination and its regulation
  • Push back to respond better: regulatory inhibition of the DNA double-strand break response
  • The DNA-damage response in human biology and disease
  • DNA strand break repair and human genetic disease
  • gammaH2AX: a sensitive molecular marker of DNA damage and repair
  • RAD51 localization and activation following DNA damage
  • The endless tale of nonhomologous end-joining
  • The DNA repair complex Ku70/86 modulates Apaf1 expression upon DNA damage
  • Rad51-deficient vertebrate cells accumulate chromosomal breaks prior to cell death
  • Down-regulation of 8-oxoguanine DNA glycosylase 1 expression in the airway epithelium ameliorates allergic lung inflammation
  • DNA glycosylases: specificity and mechanisms
  • Sequence and stacking dependence of 8-oxoguanine oxidation: comparison of one-electron vs. single oxygen mechanisms
  • Innate inflammation induced by the 8-oxoguanine DNA glycosylase-1-KRAS-NF-kappaB pathway
  • Whole transcriptome analysis reveals an 8-oxoguanine DNA glycosylase-1-driven DNA repair-dependent gene expression linked to essential biological processes
  • Innate mechanism of pollen- and cat dander-induced oxidative stress and DNA damage in the airways
  • Facilitation of allergic sensitization and allergic airway inflammation by pollen-induced innate neutrophil recruitment
  • DNA methylation of Th2 lineage determination genes at birth is associated with allergic outcomes in childhood