ArticleThe Journal of allergy and clinical immunology2014
Maternal allergy increases susceptibility to offspring allergy in association with TH2-biased epigenetic alterations in a mouse model of peanut allergy.
Article in The Journal of allergy and clinical immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 38 citations in OpenAlex.
- Maternal influences on offspring food allergy.Immunological reviews · 2024Review
- Early-life risk factors which govern pro-allergic immunity.Seminars in immunopathology · 2024Review
- Sustained silencing peanut allergy by xanthopurpurin is associated with suppression of peripheral and bone marrow IgE-producing B cell.Frontiers in immunology · 2024Article
- Pathogenesis of allergic diseases and implications for therapeutic interventions.Signal transduction and targeted therapy · 2023Review
- Asthma and the Missing Heritability Problem: Necessity for Multiomics Approaches in Determining Accurate Risk Profiles.Frontiers in immunology · 2022Review
- Epigenetics in Food Allergy and Immunomodulation.Nutrients · 2021Review
- Sensitisation patterns and allergy outcomes in pregnant women living in the urban area.Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2021Article
- DNA Methylation Levels in Mononuclear Leukocytes from the Mother and Her Child Are Associated with IgE Sensitization to Allergens in Early Life.International journal of molecular sciences · 2021Article
- Gestation and breastfeeding in schistosomotic mice differentially alters the expression of histone deacetylases (HDACs) in adult offspring.Memorias do Instituto Oswaldo Cruz · 2020Article
- Influences of Maternal Factors Over Offspring Allergies and the Application for Food Allergy.Frontiers in immunology · 2019Review
- Transgenerational and intergenerational epigenetic inheritance in allergic diseases.The Journal of allergy and clinical immunology · 2018Review
- B-FAHF-2 plus oral immunotherapy (OIT) is safer and more effective than OIT alone in a murine model of concurrent peanut/tree nut allergy.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2017Article
- Balancing Tolerance or Allergy to Food Proteins.Trends in immunology · 2016Review
- Environmentally induced epigenetic toxicity: potential public health concerns.Critical reviews in toxicology · 2016Review
- Inter- and transgenerational epigenetic inheritance: evidence in asthma and COPD?Clinical epigenetics · 2015Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundAlthough maternal atopy is a risk factor for the development of peanut allergy, this phenomenon has not been well characterized experimentally, and the mechanisms underlying offspring risk are unclear.
objectiveWe sought to determine whether offspring of mothers with peanut allergy (O-PAM mice) are more susceptible to peanut allergy than offspring of naive mothers (O-NM mice) in a murine model and, if so, whether the susceptibility is linked to TH2-biased epigenetic alterations.
methodsFive-week-old O-PAM and O-NM mice were intragastrically sensitized to and challenged with peanut. Serum peanut-specific IgE levels, plasma histamine levels, anaphylactic reactions, and splenocyte and MLN cell cytokine production were measured. DNA methylation levels of the Il4 gene promoter from splenocytes and MLN cells from sensitized offspring and splenocytes from unsensitized neonatal offspring were determined by means of pyrosequencing.
resultsO-PAM mice exhibited 3-fold higher peanut-specific IgE levels after peanut sensitization, as well as 5-fold higher histamine levels and significantly higher anaphylactic symptom scores after challenge than O-NM mice (P < .05-.01). Cultured splenocytes and MLNs from O-PAM mice produced significantly more TH2 cytokines than cells from O-NM mice (P < .05-.01). Cells from O-PAM mice exhibited significantly reduced DNA methylation at CpG sites of the Il4 gene promoter than cells from O-NM mice. DNA methylation levels were inversely correlated with IL-4 and IgE production. O-PAM neonatal splenocyte hypomethylation of the Il4 gene promoter was also present.
conclusionThis study is the first to demonstrate that increased susceptibility to peanut allergy in O-PAM mice is associated with epigenetic alteration of the Il4 gene promoter. This finding might provide insight into preventing the development of early-life allergy.
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