Epigenetic age acceleration is associated with allergy and asthma in children in Project Viva

Peng, Cheng; Cárdenas, Andrés; Rifas‐Shiman, Sheryl L.; Hivert, Marie‐France; Gold, Diane R.; Platts-Mills, Thomas A.E.; Lin, Xihong; Oken, Emily; Avila, Lydiana; Celedón, Juan C.; Weiss, Scott T.; Baccarelli, Andrea A.; Litonjua, Augusto A.; DeMeo, Dawn L.

doi:10.1016/j.jaci.2019.01.034

Cited by 45 publications

(50 citation statements)

References 54 publications

(85 reference statements)

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“…Accelerated epigenetic aging, i.e., a higher biological age predicted from the DNA methylation patterns then the true chronological age, has been associated with a large number of disease and an overall greater risk of death [67], while longevity has been associated with decelerated epigenetic aging [68]. Epigenetic aging has now also been assessed in the context of atopic or allergen sensitization and asthma using a variety of different clocks [30,69]. Accelerated epigenetic aging in children at 7-8 years of age was associated with increased serum IgE levels and a 1.2-1.3-fold increased risk of atopic sensitization, or sensitization to environmental or food allergens for every 1-year increase in epigenetic age [69].…”

Section: Environment and Epigenetics In Asthma And Allergymentioning

confidence: 99%

“…Epigenetic aging has now also been assessed in the context of atopic or allergen sensitization and asthma using a variety of different clocks [30,69]. Accelerated epigenetic aging in children at 7-8 years of age was associated with increased serum IgE levels and a 1.2-1.3-fold increased risk of atopic sensitization, or sensitization to environmental or food allergens for every 1-year increase in epigenetic age [69].…”

Section: Environment and Epigenetics In Asthma And Allergymentioning

confidence: 99%

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Recent findings in the genetics and epigenetics of asthma and allergy

Kabesch¹,

Tost

2020

Semin Immunopathol

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In asthma and allergy genetics, a trend towards a few main topics developed over the last 2 years. First, a number of studies have been published recently which focus on overlapping and/or very specific phenotypes: within the allergy spectrum but also reaching beyond, looking for common genetic traits shared between different diseases or disease entities. Secondly, an urgently needed focus has been put on asthma and allergy genetics in populations genetically different from European ancestry. This acknowledges that the majority of new asthma patients today are not white and asthma is a truly worldwide disease. In epigenetics, recent years have seen several large-scale epigenome-wide association studies (EWAS) being published and a further focus was on the interaction between the environment and epigenetic signatures. And finally, the major trends in current asthma and allergy genetics and epigenetics comes from the field of pharmacogenetics, where it is necessary to understand the susceptibility for and mechanisms of current asthma and allergy therapies while at the same time, we need to have scientific answers to the recent availability of novel drugs that hold the promise for a more individualized therapy.

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Section: Environment and Epigenetics In Asthma And Allergymentioning

confidence: 99%

Section: Environment and Epigenetics In Asthma And Allergymentioning

confidence: 99%

Recent findings in the genetics and epigenetics of asthma and allergy

Kabesch¹,

Tost

2020

Semin Immunopathol

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“…PSC risk factors that exacerbate systemic oxidative stress can be expected to accelerate aging according to the free-radical theory of aging (Harman 2003). Supportive of this premise, atopy (i.e., asthma in children), diabetes and high dose IR have been shown to advance biological age, as assessed by epigenetic markers or the common diseases of aging (Morley 2008;Richardson 2009;Peng et al 2019).…”

Section: Two-stage Psc Developmentmentioning

confidence: 99%

Etiology of posterior subcapsular cataracts based on a review of risk factors including aging, diabetes, and ionizing radiation

Richardson

Ainsbury

Prescott

et al. 2020

International Journal of Radiation Biology

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Purpose: Since the exact development of posterior subcapsular cataracts (PSCs) is poorly understood, we review various risk factors and propose a two-stage etiology for PSCs. Methods: The biological mechanisms associated with age-related cataracts (primarily nuclear cataracts, cortical cataracts and PSCs) were reviewed in relation to selected risk factors that induce PSCs (including atopy, diabetes, hypoparathyroidism, myopia, retinitis, solar radiation, steroid use, uveitis, vitrectomy and ionizing radiation). We particularly focused on ionizing radiation, as this is known to be a risk factor specific to PSCs. Based on an analysis of the reviewed material, we propose a detailed explanation of the etiology of PSCs. Conclusions: Lens epithelial cells (LECs) and lens fiber cells are normally hypoxic and therefore very sensitive to changes in oxidative stress, as quantified by the radiation oxygen effect. We hypothesize that the development of PSC opacities is a two-stage process. Stage I, early in life, is driven by risk factors that promote oxidative stress and ion-pump disruption, harming lens fibers and causing aberrant LECs to proliferate and ectopically migrate as Wedl cells (perhaps by processes associated with an epithelial to mesenchymal transition) to the posterior pole region. After a latent period, in Stage II, the development of PSCs advances mainly due to chronic inflammation and other premature aging-related mechanisms that promote mature vacuolar or plaque PSC. This two-stage hypothesis of PSC etiology accounts for risk factors, such as aging, diabetes and ionizing radiation, which directly affects LECs and the lens. In addition, these risk factors can damage other ocular regions, such as the retina and vitreous, that also indirectly contribute to the development of PSCs. It is possible that the incidence of PSCs may be reduced by reversing the effects of Stage I through various means, including ocular antioxidants.

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“…All 36 patients were Caucasian and 44% were male. The median (IQR) chronologic age at the diagnostic endoscopy for responders was 39 years 29,43 and for non-responders 35 years 26,43 (Table 1).…”

Section: Re Sultsmentioning

confidence: 99%

“…24,25 Advanced molecular age has also been associated with atopic illness. [26][27][28][29] Maternal and neonatal 25-hydroxyvitamin D concentrations have been associated with atopic illness in children, and supplemental vitamin D, during pregnancy, has been associated with methylation changes in cord blood. 30,31 Although EoE is highly associated with atopic illness, epigenetic markers in EoE have not been extensively studied.…”

Section: Introductionmentioning

confidence: 99%

Epigenetic methylation in Eosinophilic Esophagitis: Molecular ageing and novel biomarkers for treatment response

Jensen

Langefeld

Zimmerman

et al. 2020

Clin Experimental Allergy

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Background: Treatment failure in eosinophilic esophagitis (EoE) is common. We hypothesize that DNA methylation differs between patients by treatment response to topical steroids (oral viscous budesonide), thus offering the potential to inform targeting therapies. Objective: We sought to identify differentially methylated sites and affiliated genes in pre-treatment oesophageal cells between responders and non-responders and test for accelerated epigenetic ageing in oesophageal cells of EoE patients. Methods: DNA was extracted from prospectively collected and biobanked oesophageal biopsies from 36 Caucasian treatment naïve EoE patients at diagnosis. Methylation assays were completed using the Infinium HumanMethylation450 BeadChip. Normalized β values for each CpG site were tested (t test) for differential methylation. Further, 353 CpG probes were used to estimate epigenetic age for each patient and a linear regression model tested whether chronologic age and epigenetic age differed. Epigenetic age results were confirmed in an independent cohort of healthy controls. Results: Eighteen CpG sites were differentially methylated by treatment response (P < .00001). The mean epigenetic age and chronological age were 56.1 ± 11.1 and 36.7 ± 12.3 years, a mean age difference of 19.3 ± 5.2 years (P < .0001); accelerated ageing was not observed in the oesophageal cells of healthy controls. Conclusions and clinical relevance: EoE patients that respond versus do not respond to treatment have differences in their methylation profile, including enrichment of genes in pathways consistent with cellular injury and repair due to environmental stress and cell adhesion and barrier integrity. EoE also appears to accelerate cellular ageing. Whether treatment can arrest or reverse accelerated epigenetic ageing and the implications for long-term disease progression is important areas for future research.

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Epigenetic age acceleration is associated with allergy and asthma in children in Project Viva

Cited by 45 publications

References 54 publications

Recent findings in the genetics and epigenetics of asthma and allergy

Recent findings in the genetics and epigenetics of asthma and allergy

Etiology of posterior subcapsular cataracts based on a review of risk factors including aging, diabetes, and ionizing radiation

Epigenetic methylation in Eosinophilic Esophagitis: Molecular ageing and novel biomarkers for treatment response

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