233:
APRIL, BAFF, and TGF-β Concentrations in Colostrum Correlate with Allergic Disease Outcome
Saturday, March 3, 2018
South Hall A2 (Convention Center)
Puja Sood, MD, John J. Varrone, PhD, Anna K. Kukkonen, PhD, Mikael Kuitunen, MD PhD, Erkki Savilahti, MD PhD, Antti E. Seppo, PhD, Kirsi M. Jarvinen-Seppo, MD PhD FAAAAI
RATIONALE: Human milk provides passive immunity during the first weeks of life. T-cell independent (TI) stimulation may be a significant mechanism by which the infant’s naïve B-cells undergo IgA class switch recombination (CSR). The cytokines implicated in IgA CSR include IL-10, TGF-β, A Proliferation-Inducing Ligand (APRIL), and B-cell Activation Factor (BAFF). Although it has been well established that IL-10 and TGF-β are present in human breast milk, the concentrations of APRIL in human milk have not been reported.

METHODS: We utilized stored frozen colostrum samples from the previously published probiotic interventional study of pregnant mothers from Helsinki, Finland carrying children with hereditary allergic predisposition. The children born from these mothers were followed-up at 5 years for development of allergic disease. Forty-five colostrum samples were randomly selected from mothers who had children with ‘allergic disease’ and with ‘no allergic disease.’ The concentrations of cytokines were determined using Luminex.

RESULTS: The concentration of APRIL was significantly lower in children who developed food allergy (p=0.0785) or asthma (p=0.0471) compared to those who did not. The concentration of BAFF was significantly lower in infants who developed asthma (p=0.0024) or allergic rhinitis (p=0.0039) compared to those who did not. TGF-β3 concentration was significantly elevated in children who developed asthma (p=0.0100) or allergic rhinitis (p=0.0453) compared to those who did not. Probiotic supplementation did not impact cytokine levels.

CONCLUSIONS: Increased APRIL and BAFF concentrations in colostrum may be associated with protection against onset of allergic disease in early life, possibly due to the impact of these cytokines on IgA production.