Fatty acids in cord blood plasma, the relation to soluble CD23 and subsequent atopy

Kristine Byberg1, Knut Øymar, Lage Aksnes

  • 1Department of Pediatrics, Stavanger University Hospital, Stavanger, Norway.

Insights

Lower levels of omega-3 polyunsaturated fatty acids (PUFAs) in cord blood may increase the risk of developing atopy in children. This suggests a link between n-3 PUFA levels and the development of allergic conditions.

Area of Science:

  • Immunology
  • Nutritional Science
  • Pediatrics

Background:

  • Atopy, a predisposition to allergic diseases, is potentially linked to the dietary balance of omega-6 (n-6) and omega-3 (n-3) long-chain polyunsaturated fatty acids (PUFAs).
  • Soluble low affinity IgE receptor (sCD23) plays a role in IgE regulation and allergic responses.

Purpose of the Study:

  • To investigate the association between cord blood levels of fatty acids, IgE, and sCD23 and the subsequent development of atopy in children.
  • To explore the potential role of n-3 PUFAs in the development of allergic sensitization and atopic dermatitis.

Main Methods:

  • A nested case-control study involving 70 children (35 with subsequent atopy, 35 matched controls without atopy).
  • Measurement of fatty acid profiles, IgE, and sCD23 levels in cord blood plasma.
  • Statistical analysis to identify correlations between these biomarkers and the development of atopy.

Main Results:

  • A trend towards lower levels of n-3 PUFAs, specifically eicosapentaenoic acid (EPA) and alpha-linolenic acid (ALA), was observed in the cord blood of children who later developed atopy.
  • sCD23 levels showed a negative correlation with n-3 PUFAs and n-9 eicosenoic acid.
  • n-9 eicosenoic acid levels were negatively correlated with IgE levels, while no association was found between sCD23 and n-6 PUFAs.

Conclusions:

  • Lower concentrations of n-3 PUFAs in cord blood may be associated with an increased risk of developing atopy in children.
  • A potential mechanism involves the regulation of CD23 by n-3 PUFAs, influencing IgE synthesis and allergic development.