Food-Specific Immunoglobulin a Does Not Correlate With Natural Tolerance to Peanut or Egg Allergens

Characterization of infant gut food-specific immunoglobulin A (IgA) responses and the assessment of correlation between peanut-and/or egg white-specific IgA with clinical measures of food tolerance.

The study included 112 stool samples from 51 infants with no clinical history of food allergy nor food protein-induced allergic proctocolitis from the GMAP study. The study population further included 441 stool and 330 plasma samples at enrollment and 124 stool and 84 plasma samples at follow-up from atopic nonpeanut allergic infants within the CoFAR2 cohort, 9 stool samples from peanut-allergic patients from the POISED trial, and 9 fecal samples from healthy nonallergic individuals from the Stanford Twin Registry.

This is a laboratory-based exploratory analytical study. Enzyme-linked immunosorbent assays were used to quantitate stool peanut- and egg white-specific IgA and plasma peanut-specific IgA. Fecal IgA was used as a proxy for gut IgA for practical purposes. Bead-based epitope assays were used to investigate epitope specificity between immunoglobin subtypes and isotypes, respectively.

There was no statistically significant difference (P = .34) in stool peanut-specific IgA levels between infants who were avoiding and consuming peanut and there was no relationship discovered between stool or plasma peanut-specific IgA and peanut-specific IgE measures, skin prick test score, nor clinical allergy among unsensitized infants (P >.05). There was no relationship between baseline total stool egg white-specific IgA levels and oral food challenge-proven tolerance to egg, nor was there a statistically significant difference in total stool egg white-specific IgA levels between egg-allergic and nonallergic children at follow-up (P = .43).

There was no correlation between gut peanut-specific IgA with concurrent peanut sensitization nor allergy and peanut-specific IgA was not correlated with oral food challenge-proven tolerance to peanut. Gut peanut-specific IgA was also demonstrated to have different epitope specificity compared with plasma peanut-specific IgE. Egg white-specific IgA was detectable in infant stool; however, it was nonpredictive for egg tolerance nor egg allergy outgrowth.

The prevalence of pediatric food allergies is increasing, and it has been commonly hypothesized that gut food-specific IgA may play a protective role by neutralizing ingested food antigens and preventing IgE sensitization. This study provides evidence directly challenging a commonly held belief regarding a potentially tolerogenic role of gut food-specific IgA and further illuminates a need for future studies to investigate early-life events that differentially lead to the production of food-specific IgA and IgE, respectively.