Recognition of Human Milk Peptides by IgE Antibodies from Infants with Cow's Milk Allergy

Abstract

RationaleOccasionally, exclusively breastfed, cow's milk-allergic infants continue to be symptomatic despite strict maternal milk avoidance. We sought to determine whether this phenomenon could be due to sensitization against human milk proteins.MethodsWe generated ten peptides (10-12 amino acid in length), representing known bovine milk IgE-binding epitopes of alpha-lactalbumin, beta-, and kappa-casein and the corresponding, highly similar human milk peptides (differing by 1 to 5 amino acids) on the SPOT membranes. The peptides were labeled with sera from 9 breastfed milk-allergic infants (milk-IgE <0.35 to 15.9 kUA/L) who were asymptomatic and 6 infants (milk IgE 100 kUA/L) who were symptomatic during maternal milk-elimination diet; aged 3 weeks to 12 months.ResultsHuman milk peptides were generally less often bound by IgE from milk-allergic infants than the homologous bovine milk peptides. Nine patients had peptide-specific IgE to human alpha-lactalbumin, four to human beta-casein and twelve to human kappa-casein. At least one human milk peptide was strongly bound by IgE from 4/6 symptomatic infants and by 3/9 asymptomatic infants. Interestingly, two infants who were symptomatic while their mothers avoided cow's milk had IgE specific to a human beta-casein peptide but none or little to the corresponding bovine counterpart.ConclusionsThese data suggest that human milk proteins are recognized by the IgE from the majority of milk-allergic infants who continue having symptoms despite maternal milk avoidance, although some asymptomatic infants also possess some human milk-specific IgE. The clinical significance of these IgE antibodies requires further investigation in a functional assay. RationaleOccasionally, exclusively breastfed, cow's milk-allergic infants continue to be symptomatic despite strict maternal milk avoidance. We sought to determine whether this phenomenon could be due to sensitization against human milk proteins. Occasionally, exclusively breastfed, cow's milk-allergic infants continue to be symptomatic despite strict maternal milk avoidance. We sought to determine whether this phenomenon could be due to sensitization against human milk proteins. MethodsWe generated ten peptides (10-12 amino acid in length), representing known bovine milk IgE-binding epitopes of alpha-lactalbumin, beta-, and kappa-casein and the corresponding, highly similar human milk peptides (differing by 1 to 5 amino acids) on the SPOT membranes. The peptides were labeled with sera from 9 breastfed milk-allergic infants (milk-IgE <0.35 to 15.9 kUA/L) who were asymptomatic and 6 infants (milk IgE 100 kUA/L) who were symptomatic during maternal milk-elimination diet; aged 3 weeks to 12 months. We generated ten peptides (10-12 amino acid in length), representing known bovine milk IgE-binding epitopes of alpha-lactalbumin, beta-, and kappa-casein and the corresponding, highly similar human milk peptides (differing by 1 to 5 amino acids) on the SPOT membranes. The peptides were labeled with sera from 9 breastfed milk-allergic infants (milk-IgE <0.35 to 15.9 kUA/L) who were asymptomatic and 6 infants (milk IgE 100 kUA/L) who were symptomatic during maternal milk-elimination diet; aged 3 weeks to 12 months. ResultsHuman milk peptides were generally less often bound by IgE from milk-allergic infants than the homologous bovine milk peptides. Nine patients had peptide-specific IgE to human alpha-lactalbumin, four to human beta-casein and twelve to human kappa-casein. At least one human milk peptide was strongly bound by IgE from 4/6 symptomatic infants and by 3/9 asymptomatic infants. Interestingly, two infants who were symptomatic while their mothers avoided cow's milk had IgE specific to a human beta-casein peptide but none or little to the corresponding bovine counterpart. Human milk peptides were generally less often bound by IgE from milk-allergic infants than the homologous bovine milk peptides. Nine patients had peptide-specific IgE to human alpha-lactalbumin, four to human beta-casein and twelve to human kappa-casein. At least one human milk peptide was strongly bound by IgE from 4/6 symptomatic infants and by 3/9 asymptomatic infants. Interestingly, two infants who were symptomatic while their mothers avoided cow's milk had IgE specific to a human beta-casein peptide but none or little to the corresponding bovine counterpart. ConclusionsThese data suggest that human milk proteins are recognized by the IgE from the majority of milk-allergic infants who continue having symptoms despite maternal milk avoidance, although some asymptomatic infants also possess some human milk-specific IgE. The clinical significance of these IgE antibodies requires further investigation in a functional assay. These data suggest that human milk proteins are recognized by the IgE from the majority of milk-allergic infants who continue having symptoms despite maternal milk avoidance, although some asymptomatic infants also possess some human milk-specific IgE. The clinical significance of these IgE antibodies requires further investigation in a functional assay.