Effect of prenatal antioxidant intake on infants' respiratory infection is modified by a CD14 polymorphism

Seo Ah Hong1, Eun Lee2, Sung Ok Kwon3

  • 1ASEAN Institute for Health Development, Mahidol University, Salaya, Phutthamonthon, Nakhonpathom, Thailand.

Insights

Prenatal antioxidant intake may protect infants from respiratory tract infections (RTIs). This protective effect is influenced by specific genetic variations in immunity genes like CD14, TLR4, and GSDMB.

Area of Science:

  • Environmental influences on child health
  • Nutritional epidemiology
  • Immunogenetics

Background:

  • Prenatal maternal diet impacts offspring disease susceptibility, particularly with specific genetic predispositions.
  • Immunity gene polymorphisms may interact with prenatal nutrition to affect infant health outcomes.

Purpose of the Study:

  • To investigate the interaction between prenatal antioxidant intake and specific immunity gene polymorphisms (CD14, TLR4, GSDMB) on infant respiratory tract infection (RTI) susceptibility at 12 months.
  • To determine if maternal diet during pregnancy influences RTI risk in infants based on their genetic makeup.

Main Methods:

  • Analysis of 550 infants from the Cohort for Childhood Origin of Asthma and Allergic Diseases (COCOA) birth cohort.
  • Assessment of prenatal maternal diet using a food frequency questionnaire.
  • Genotyping of infant cord blood for CD14 (rs2569190), TLR4 (rs1927911), and GSDMB (rs4794820) polymorphisms.

Main Results:

  • Higher prenatal intake of fruits and vegetables (FV) correlated with decreased RTI risk.
  • Specific genotypes (e.g., TT at rs2569190) showed reduced RTI risk with higher prenatal vitamin A, C, and FV intake.
  • Interactions were observed between prenatal antioxidant intake and polymorphisms in CD14, TLR4, and GSDMB, modifying RTI risk.

Conclusions:

  • Prenatal antioxidant intake may offer protection against infant RTIs.
  • The relationship between prenatal antioxidant intake and RTI risk is significantly modified by CD14, TLR4, and GSDMB gene polymorphisms.
Abstract