Secretory Antibodies to Cow Milk Proteins and to Respiratory Syncytial Virus

The failure of early studies to detect IgA on mucosal membranes and the lack of a reason to assume the presence of secretory antibody for many years preserved the dogma that mucosal membranes are without specific protection at the time of birth. In recent years secretory IgA (S-IgA) and IgM antibodies to Escherichia coli, to poliovirus type I and to milk proteins have been identified in the saliva of newborn infants1,2. S-IgA anti-β-lactoglobulin (BLG) and S-IgA anti-casein (Cas) were found independently of the mode of feeding, could be specifically blocked but were not blocked by preincubation with unrelated protein. In a subsequent study in which 158 infants were investigated, such antibodies were shown to be consistently present3; IgA accounted for the majority of specific binding. Comparison of infants with and without risk of allergy showed a significantly higher salivary S-IgA anti-Cas in infants at risk for allergy. In a follow-up of these 158 infants over 3 and 6 months of age, breast-fed infants had significantly lower antibody titers than formula-fed infants. This was unrelated to the amount of cow protein antigen received by the infants; breastfeeding of even 1–3 weeks duration resulted in suppression of S-IgA antibody formation4. The following paper will describe the relationship between elevated concentrations of anti-Cas antibodies at birth and the appearance of atopic disease during the first year of life. Data will also be shown from a second group of 108 infants whose secretory antibody response to respiratory syncytial virus (RSV) was determined at birth, 3 months, 6 months and 1 year of age.