Childhood Asthma Atopy Center

Seoul, South Korea

Childhood Asthma Atopy Center

Seoul, South Korea
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Lee J.-Y.,Childhood Asthma Atopy Center | Lee J.-Y.,University of Ulsan | Seo J.-H.,Childhood Asthma Atopy Center | Seo J.-H.,University of Ulsan | And 10 more authors.
International Archives of Allergy and Immunology | Year: 2012

Background: The aims of this study were to determine (1) the prevalence of atopic dermatitis (AD) in Seoul, Korea, and (2) the influence of environmental and genetic factors on disease risk. Methods: A questionnaire survey was conducted in 5,036 primary school children and 4,607 middle school children in 2008. For each child, a modified version of the International Study of Asthma and Allergies in Childhood (ISAAC) questionnaire and a questionnaire assessing exposure to environmental variables were completed. Results: In primary school children, the lifetime prevalence of itchy eczema was 24.3%, the 12-month prevalence of itchy flexural eczema was 18.0%, the lifetime prevalence of AD diagnosis was 31.3%, and the 12-month prevalence of AD treatment was 14.5%. In middle school children, the corresponding rates were 16.0, 10.8, 22.1, and 8.3%, respectively. These rates are significantly higher than those reported in similar studies conducted in 1995 and 2000. In both primary and middle school children, a parental history of allergic disease and a history of having moved into a newly built house before 1 year of age were independently associated with a risk for current AD. For current AD, the prevalence odds ratio was higher in the subgroup with both a genetic and a specific environmental risk factor than in the subgroup with no risk factor or subgroups with only one risk factor. Conclusions: The prevalence of AD in primary and middle school children in Seoul has increased. Its development may be influenced by gene-environment interactions, particularly before 1 year of age. Copyright © 2011 S. Karger AG, Basel.


Lee S.-Y.,Hallym University | Yu J.,Childhood Asthma Atopy Center | Ahn K.-M.,Sungkyunkwan University | Kim K.W.,Yonsei University | And 24 more authors.
PLoS ONE | Year: 2014

Background: Although cesarean delivery and prenatal exposure to antibiotics are likely to affect the gut microbiome in infancy, their effect on the development of atopic dermatitis (AD) in infancy is unclear. The influence of individual genotypes on these relationships is also unclear. To evaluate with a prospective birth cohort study whether cesarean section, prenatal exposure to antibiotics, and susceptible genotypes act additively to promote the development of AD in infancy. Methods: The Cohort for Childhood of Asthma and Allergic Diseases (COCOA) was selected from the general Korean population. A pediatric allergist assessed 412 infants for the presence of AD at 1 year of age. Their cord blood DNA was subjected to interleukin (IL)-13 (rs20541) and cluster-of-differentiation (CD)14 (rs2569190) genotype analysis. Results: The combination of cesarean delivery and prenatal exposure to antibiotics associated significantly and positively with AD (adjusted odds ratio, 5.70; 95% CI, 1.19-27.3). The association between cesarean delivery and AD was significantly modified by parental history of allergic diseases or risk-associated IL-13 (rs20541) and CD14 (rs2569190) genotypes. There was a trend of interaction between IL-13 (rs20541) and delivery mode with respect to the subsequent risk of AD. (P for interaction = 0.039) Infants who were exposed prenatally to antibiotics and were born by cesarean delivery had a lower total microbiota diversity in stool samples at 6 months of age than the control group. As the number of these risk factors increased, the AD risk rose (trend p<0.05). Conclusion: Cesarean delivery and prenatal antibiotic exposure may affect the gut microbiota, which may in turn influence the risk of AD in infants. These relationships may be shaped by the genetic predisposition. © 2014 Lee et al.


Oh M.-A.,Samsung | Shim J.Y.,Sungkyunkwan University | Jung Y.-H.,Childhood Asthma Atopy Center | Seo J.-H.,Childhood Asthma Atopy Center | And 14 more authors.
Pediatric Pulmonology | Year: 2013

Background Asthma is a chronic lower airway inflammatory disease. Nitric oxide is an inflammatory mediator produced endogenously in the airway. Previous studies have demonstrated that the fractional concentration of exhaled nitric oxide (FeNO) is increased in asthma. Objectives To investigate if FeNO concentrations were correlated with wheezing phenotypes in preschool children and to compare the FeNO results with airway hyperresponsiveness (AHR) and pulmonary function test (PFT) results. Methods We performed skin prick tests, methacholine provocation tests, PFT, impulse oscillometry bronchodilator response (IOS BDR) tests, and FeNO measurements in 372 preschool children between the ages of 4 and 6 years. Wheezing phenotypes were defined according to the age of onset and persistency. Results Persistent wheezers had higher FeNO levels than transient wheezers and non-wheezers. Among persistent wheezers, those with atopy and AHR had significantly higher FeNO levels than those without atopy or AHR. FeNO levels were significantly higher in late-onset wheezers than early-onset wheezers and non-wheezers. Among late-onset wheezers, those with atopy and AHR had a significantly higher FeNO concentration than those without atopy or AHR as well as those with either atopy or AHR. However, there were no significant differences in AHR, PFT, or IOS BDR between persistent and transient wheezers or between late-onset wheezers and early-onset wheezers. Conclusion FeNO may be a better marker for asthma phenotypes in preschool children than AHR and PFT results. Pediatr Pulmonol. 2013; 48:563-570. © 2012 Wiley Periodicals, Inc. Copyright © 2012 Wiley Periodicals, Inc.


Kang M.-J.,A-Life Medical | Yu H.-S.,A-Life Medical | Seo J.-H.,Korea Cancer Center Hospital | Kim H.-Y.,University of Ulsan | And 6 more authors.
Human Immunology | Year: 2012

In 2007, a genome-wide association study identified associations between variants involved in the regulation of ORMDL3 expression and asthma. These observations were subsequently replicated in case-control studies in several ethnic groups. We investigated the possible contribution of GSDMB/ORMDL3 variants to asthma susceptibility and intermediate asthma phenotypes in Korean children. The polymorphisms rs7216389, rs4794820, rs4065275, and rs11650680 were genotyped using the TaqMan assay in 931 asthmatics and 480 normal controls in a case-control study, and in 1907 elementary school children in a general population study. Each subject also underwent peripheral blood analysis of immunoglobulin E levels, eosinophil cationic protein (ECP) levels, and eosinophil percentage. Pulmonary function testing (FEV1 and MMEF) and a methacholine provocation test (PC20) were also performed. The case-control study revealed a significant association between a linkage disequilibrium block, including rs7216389, rs4794820, and rs4065275, and susceptibility to asthma and atopic asthma. The CT and TT genotypes of rs11650680 were associated with lower logECP levels than the CC genotype in asthmatics, while the GA and AA genotypes of rs4794820 were associated with higher logPC20 values than the GG genotype in atopic asthmatics. The haplotype (CAA) of rs7216389, rs4794820 and rs4065275 was associated with a lower risk of asthma susceptibility and a higher logPC20. In the general population study, rs11650680 was significantly associated with a diagnosis of asthma. Moreover, the GA and AA genotypes of rs4794820 were associated with higher logPC20 values and lower eosinophil percentages than the GG genotype in subjects who had been diagnosed with asthma, or showed bronchial hyperresponsiveness (PC2016). The GSDMB/ORMDL3 gene block, which includes rs7216389, rs4065275, rs4794820, and rs11650680, may be associated with asthma susceptibility in Korean children because it promotes eosinophilic inflammation, which induces bronchial hyperresponsiveness. © 2012 American Society for Histocompatibility and Immunogenetics.


Kim H.-J.,University of Ulsan | Lee E.,Childhood Asthma Atopy Center | Lee E.,University of Ulsan | Lee S.-H.,University of Ulsan | And 3 more authors.
Clinical Immunology | Year: 2015

Mold has been implicated in the development of atopic dermatitis (AD); however, the underlying mechanisms remain unknown. The aim of the study was to investigate the effects of mold exposure in early life through epidemiologic and mechanistic studies in vivo and in vitro. Exposure to visible mold inside the home during the first year of life was associated with an increased risk for current AD by two population-based cross-sectional human studies. Children with the AG + GG genotype of GSTP1 showed increased risk for current AD when exposed to mold. In the mouse model, treatment with patulin induced and aggravated clinically significant AD and Th2-related inflammation of the affected mouse skin. Additionally, reactive oxygen species (ROS) were released in the mouse skin as well by human keratinocytes. In conclusions, mold exposure increases the risk for AD related to ROS generation mediated by Th2-promoting inflammatory cytokines. © 2015 Elsevier Inc.

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