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Additive effect between IL-13 polymorphism and cesarean section delivery/prenatal antibiotics use on atopic

So-Yeon Lee1, Jinho Yu2, Kang-Mo Ahn3

  • 1Department of Pediatrics, Hallym University College of Medicine, Anyang, Korea.

Plos One
|May 23, 2014
PubMed

Insights

Cesarean delivery and prenatal antibiotic exposure increase infant atopic dermatitis risk, especially with specific genetic factors. Gut microbiome diversity is reduced in infants with both risk factors.

Area of Science:

  • Pediatric Allergy and Immunology
  • Microbiome Research
  • Genetics and Disease

Background:

  • Cesarean delivery and prenatal antibiotic exposure are known to influence infant gut microbiome development.
  • The specific impact of these factors and genetic predispositions on infant atopic dermatitis (AD) risk remains unclear.

Purpose of the Study:

  • To investigate the combined effects of cesarean delivery, prenatal antibiotic exposure, and specific genotypes on the development of atopic dermatitis in infancy.
  • To explore the additive influence of these risk factors on AD development.

Main Methods:

  • A prospective birth cohort study (COCOA) of 412 Korean infants was conducted.
  • Infant AD was assessed at 1 year, and cord blood DNA was analyzed for IL-13 (rs20541) and CD14 (rs2569190) genotypes.
  • Stool microbiota diversity was analyzed at 6 months in a subset of infants.

Main Results:

  • Cesarean delivery combined with prenatal antibiotic exposure significantly increased AD risk (aOR 5.70).
  • Genetic factors (IL-13, CD14) and parental allergy history modified the association between cesarean delivery and AD.
  • Infants with both cesarean delivery and prenatal antibiotic exposure showed reduced gut microbiota diversity and a dose-response increase in AD risk with more risk factors.

Conclusions:

  • Cesarean delivery and prenatal antibiotic exposure may contribute to AD development via gut microbiota alterations.
  • Genetic predisposition plays a role in shaping these relationships and influencing infant AD risk.
Abstract

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