Allergy Asthma Respir Dis.  2013 Jun;1(2):129-137. 10.4168/aard.2013.1.2.129.

Gene-environment interaction between Toll-like receptor 4 and mold exposure in the development of atopic dermatitis in preschool children

Affiliations
  • 1Department of Pediatrics, Kosin University Gospel Hospital, Kosin University College of Medicine, Busan, Korea.
  • 2Research Center for Standardization of Allergic Diseases, Asan Medical Center, Seoul, Korea. sjhong@amc.seoul.kr
  • 3Department of Pediatrics, Childhood Asthma Atopy Center, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea.
  • 4Goucher College, Baltimore, MD, USA.
  • 5Department of Pediatrics, National Health Insurance Corporation Ilsan Hospital, Goyang, Korea.
  • 6Department of Pediatrics, Korea Cancer Center Hospital, Seoul, Korea.
  • 7Department of Pediatrics, Seoul National University Bundang Hospital, Seongnam, Korea.
  • 8Department of Pediatrics, Inje University Haeundae Paik Hospital, Busan, Korea.
  • 9Department of Pediatrics, Inje University Sanggye Paik Hospital, Seoul, Korea.
  • 10Department of Pediatrics, Hallym University Sacred Heart Hospital, Hallym University College of Medicine, Anyang, Korea.
  • 11Department of Pediatrics, Korea University College of Medicine, Seoul, Korea.
  • 12Department of Pediatrics, Inje University Seoul Paik Hospital, Seoul, Korea.
  • 13Department of Pediatrics, Kangbuk Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea.
  • 14Asan Institute for Life Sciences, Asan Medical Center, Seoul, Korea.

Abstract

PURPOSE
Genetic factors and environmental exposures are recognized as important risk factors for atopic dermatitis (AD) in children. Inflammatory responses by molds can be mediated via Toll-like receptor 4 (TLR4). The aims of this study were to investigate mold as risk factor of AD and gene-environment interaction on AD in preschool children.
METHODS
We undertook a cross-sectional survey with 986 preschool children. We investigated five mold exposure measures (dampness stain, dampness damage, visible mold, mold odor, and house repair). The TLR4 polymorphism (rs1927911) was genotyped by TaqMan assay.
RESULTS
The prevalence of AD was as follows: AD diagnosis by questionnaire, 35.1%; current AD (lifetime diagnosis together with symptoms in the last 12 months), 21.5%. When children with parental history of AD were exposed to mold odor during infancy and house repair during the last 12 months, the risk for current AD (adjusted odds ratio [aOR], 6.826; 95% confidence interval [CI], 2.511 to 18.554 vs. aOR, 6.143; 95% CI, 2.348 to 16.074) was further increased than only with parental history of AD. In children with the CC genotype of TLR4 polymorphism, the risk of AD was increased by mold exposure.
CONCLUSION
This investigation identified that mold exposure is potential risk factor for AD in preschool children. Parental history of AD and mold exposure during infancy and the last 12 months had synergistic effect on high prevalence of AD. We identified that mold exposure and TLR4 polymorphism have an effect on the development of atopic dermatitis.

Keyword

Atopic dermatitis; Mold; Risk factor; Toll-like receptor 4; Polymorphism

MeSH Terms

Child
Child, Preschool
Cross-Sectional Studies
Dermatitis, Atopic
Environmental Exposure
Fungi
Gene-Environment Interaction
Genotype
Humans
Odds Ratio
Odors
Parents
Prevalence
Risk Factors
Toll-Like Receptor 4
Toll-Like Receptors
Surveys and Questionnaires
Toll-Like Receptor 4
Toll-Like Receptors

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