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July 20, 2013
Rhinitis patients with sputum eosinophilia show decreased lung function in the absence of airway hyperresponsiveness.
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Differential epigenome-wide DNA methylation patterns in childhood obesity-associated asthma
Differential epigenome-wide DNA methylation patterns in childhood obesity-associated asthma
- Scientific Reports
- 3,
- Article number:
- 2164
- doi:10.1038/srep02164
- Received
- Accepted
- Published
- Scientific Reports
- 3,
- Article number:
- 2164
- doi:10.1038/srep02164
- Received
- Accepted
- Published
Article tools
While DNA methylation plays a role in T-helper (Th) cell maturation, its potential dysregulation in the non-atopic Th1-polarized systemic inflammation observed in obesity-associated asthma is unknown. We studied DNA methylation epigenome-wide in peripheral blood mononuclear cells (PBMCs) from 8 obese asthmatic pre-adolescent children and compared it to methylation in PBMCs from 8 children with asthma alone, obesity alone and healthy controls. Differentially methylated loci implicated certain biologically relevant molecules and pathways. PBMCs from obese asthmatic children had distinctive DNA methylation patterns, with decreased promoter methylation of CCL5, IL2RA and TBX21, genes encoding proteins linked with Th1 polarization, and increased promoter methylation of FCER2, a low-affinity receptor for IgE, and of TGFB1, inhibitor of Th cell activation. T-cell signaling and macrophage activation were the two primary pathways that were selectively hypomethylated in obese asthmatics. These findings suggest that dysregulated DNA methylation is associated with non-atopic inflammation observed in pediatric obesity-associated asthma.
Subject terms:
While DNA methylation plays a role in T-helper (Th) cell maturation, its potential dysregulation in the non-atopic Th1-polarized systemic inflammation observed in obesity-associated asthma is unknown. We studied DNA methylation epigenome-wide in peripheral blood mononuclear cells (PBMCs) from 8 obese asthmatic pre-adolescent children and compared it to methylation in PBMCs from 8 children with asthma alone, obesity alone and healthy controls. Differentially methylated loci implicated certain biologically relevant molecules and pathways. PBMCs from obese asthmatic children had distinctive DNA methylation patterns, with decreased promoter methylation of CCL5, IL2RA and TBX21, genes encoding proteins linked with Th1 polarization, and increased promoter methylation of FCER2, a low-affinity receptor for IgE, and of TGFB1, inhibitor of Th cell activation. T-cell signaling and macrophage activation were the two primary pathways that were selectively hypomethylated in obese asthmatics. These findings suggest that dysregulated DNA methylation is associated with non-atopic inflammation observed in pediatric obesity-associated asthma.
Subject terms:
At a glance
Introducing solid food: Age of introduction and its effect on risk of food allergy and other atopic diseases
Introducing solid food
Age of introduction and its effect on risk of food allergy and other atopic diseases
- Elissa Michele Abrams, MD FRCPC⇑
- Correspondence: Dr Elissa Michele Abrams, Section of Allergy and Clinical Immunology, University of Manitoba, FE125-685 William Ave, Winnipeg, MB R3E 1B2; telephone 204 787-2470; e-mail umabrams@cc.umanitoba.ca
- Allan B. Becker, MD FRCPC
- Elissa Michele Abrams, MD FRCPC⇑
- Correspondence: Dr Elissa Michele Abrams, Section of Allergy and Clinical Immunology, University of Manitoba, FE125-685 William Ave, Winnipeg, MB R3E 1B2; telephone 204 787-2470; e-mail umabrams@cc.umanitoba.ca
- Allan B. Becker, MD FRCPC
This Article
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Canadian Family PhysicianJuly 2013 vol. 59 no. 7721-722
- Canadian Family PhysicianJuly 2013 vol. 59 no. 7721-722
July 19, 2013
TSE Diagnostics: Recent Advances in Immunoassaying Prions
Clinical and Developmental Immunology
Volume 2013 (2013), Article ID 360604, 8 pages
http://dx.doi.org/10.1155/2013/360604
Review Article
TSE Diagnostics: Recent Advances in Immunoassaying Prions
Department for Production of Diagnostic Reagents and Research, Blood Transfusion Centre of Slovenia, Šlajmerjeva 6, 1000 Ljubljana, Slovenia
Received 15 March 2013; Revised 27 May 2013; Accepted 2 July 2013
Academic Editor: Benaissa El Moualij
Copyright © 2013 Anja Lukan et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract
Transmissible spongiform encephalopathies (TSEs) or prion diseases are a group of rare fatal neurodegenerative diseases, affecting humans and animals. They are believed to be the consequence of the conversion of the cellular prion protein to its aggregation-prone, β-sheet-rich isoform, named prion. Definite diagnosis of TSEs is determined post mortem. For this purpose, immunoassays for analyzing brain tissue have been developed. However, the ultimate goal of TSE diagnostics is an ante mortem test, which would be sensitive enough to detect prions in body fluids, that is, in blood, cerebrospinal fluid, or urine. Such a test would be of paramount importance also for screening of asymptomatic carriers of the disease with the aim of increasing food, drugs, and blood-derived products safety. In the present paper, we have reviewed recent advances in the development of immunoassays for the detection of prions.
Obesity and Asthma: Physiological Perspective
Journal of Allergy
Volume 2013 (2013), Article ID 198068, 11 pages
http://dx.doi.org/10.1155/2013/198068
Review Article
Obesity and Asthma: Physiological Perspective
Chest Research Foundation, Marigold Complex, Kalyani Nagar, Pune, Maharashtra 411014, India
Received 20 February 2013; Revised 27 May 2013; Accepted 3 July 2013
Academic Editor: Anurag Agrawal
Copyright © 2013 Bill Brashier and Sundeep Salvi. This is an open access article distributed under theCreative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract
Obesity induces some pertinent physiological changes which are conducive to either development of asthma or cause of poorly controlled asthma state. Obesity related mechanical stress forces induced by abdominal and thoracic fat generate stiffening of the lungs and diaphragmatic movements to result in reduction of resting lung volumes such as functional residual capacity (FRC). Reduced FRC is primarily an outcome of decreased expiratory reserve volume, which pushes the tidal breathing more towards smaller high resistance airways, and consequentially results in expiratory flow limitation during normal breathing in obesity. Reduced FRC also induces plastic alteration in the small collapsible airways, which may generate smooth muscle contraction resulting in increased small airway resistance, which, however, is not picked up by spirometric lung volumes. There is also a possibility that chronically reduced FRC may generate permanent adaptation in the very small airways; therefore, the airway calibres may not change despite weight reduction. Obesity may also induce bronchodilator reversibility and diurnal lung functional variability. Obesity is also associated with airway hyperresponsiveness; however, the mechanism of this is not clear. Thus, obesity has effects on lung function that can generate respiratory distress similar to asthma and may also exaggerate the effects of preexisting asthma.
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