Maternal Influences and Intervention Strategies on the Development of Food Allergy in Offspring

Abstract

Food allergies and other immune-mediated diseases have become serious health concerns amongst infants and children in developed and developing countries. The absence of available cures limits disease management to allergen avoidance and symptomatic treatments. Research has suggested that the presence of maternal food allergies may expose the offspring to genetic predisposition, making them more susceptible to allergen sensitization. The following review has focused on epidemiologic studies regarding maternal influences of proneness to develop food allergy in offspring. The search strategy was “food allergy OR maternal effects OR offspring OR prevention”. A systematically search from PubMed/MEDLINE, Science Direct and Google Scholar was conducted. Specifically, it discussed the effects of maternal immunity, microbiota, breastfeeding, genotype and allergy exposure on the development of food allergy in offspring. In addition, several commonly utilized prenatal and postpartum strategies to reduce food allergy proneness were presented, including early diagnosis of high-risk infants and various dietary interventions.

The clinical and immunological basis of early food introduction in food allergy prevention

“…These studies support the hypothesis that early sensitization, even in utero, can occur ( 30 , 37 , 39 , 40 ). The FONIA study of Bullens et al showed that sensitization as early as at birth (total IgE levels of ≥0.35 kU/L) was significantly associated with the development of early allergy before the age of 2 years.…”

“…Not only are IgE and IgG4 important to predict reactivity to an allergen or to confirm food tolerance, also the ratio of IgE to IgG4 seems to play a key role ( 40 , 46 ). Okamoto et al studied the concentrations of hen’s egg sIgE and IgG4 antibodies during oral food challenges (OFC) with egg white in children sensitized to hen’s egg.…”

Maternal Diet and Infant Risk of Eczema and Food Allergy: A Systematic Review

“…It is well known that maternal immunoglobulin G (IgG) is the only Ig that can pass through the placental membrane and provide passive immunity to the fetus, which is modulated by the neonatal Fc receptor (FcRn) present in the placental barrier [ 22 - 23 ]. For instance, infection during pregnancy influences the offspring's immunity through the activity of Th1/Th2 cytokines and the fetal-maternal immune transfer [ 17 ].…”

“…Individuals with allergy tolerance have much greater allergen-specific IgG4/IgE ratios than do those with allergy-prone [ 24 ]. The reasoning for this finding is that non-atopic mothers fabricate high levels of IgG1 and IgG3 antibodies that cross the placenta and confer protection to the fetus, whereas atopic mothers produce high levels of IgE and IgG4 antibodies that cannot cross the placental barrier [ 17 ]. The newborn may be predisposed for allergy sensitization and show early allergy symptoms if fetal IgE is improperly suppressed by the low maternal production of IgG1 and IgG3 [ 17 ].…”

“…The reasoning for this finding is that non-atopic mothers fabricate high levels of IgG1 and IgG3 antibodies that cross the placenta and confer protection to the fetus, whereas atopic mothers produce high levels of IgE and IgG4 antibodies that cannot cross the placental barrier [ 17 ]. The newborn may be predisposed for allergy sensitization and show early allergy symptoms if fetal IgE is improperly suppressed by the low maternal production of IgG1 and IgG3 [ 17 ]. Even though the crucial role of maternal allergen transmission and offspring risk of developing allergies is not fully understood [ 25 ], it is accepted that an immune complex made up of IgG and an allergen can be transferred from the mother to the fetus [ 25 ].…”