Abstract
Food allergy is associated with alterations in the gut microbiota, epithelial barrier, and immune tolerance. These dysfunctions are observed within the first months of life, indicating that early intervention is crucial for disease prevention. Preventive nutritional strategies with prebiotics are an attractive option, as prebiotics such as galacto-oligosaccharides and inulin can promote tolerance, epithelial barrier reinforcement, and gut microbiota modulation. Nonetheless, the ideal period for intervention remains unknown. Here, we investigated whether galacto-oligosaccharide/inulin supplementation during gestation could protect offspring from wheat allergy development in BALB/cJRj mice. We demonstrated that gestational prebiotic supplementation promoted the presence of beneficial strains in the fecal microbiota of dams during gestation and partially during mid-lactation. This specific microbiota was transferred to their offspring and maintained to adulthood. The presence of B and T regulatory immune cell subsets was also increased in the lymph nodes of offspring born from supplemented mothers, suggestive of a more tolerogenic immune environment. Indeed, antenatal prebiotic supplementation reduced the development of wheat allergy symptoms in offspring. Our study thus demonstrates that prebiotic supplementation during pregnancy induces, in the offspring, a tolerogenic environment and a microbial imprint that mitigates food allergy development.
Highlights
Food allergy (FA) is a common non-communicable disease that affects up to 10% of infants in some countries and has been increasing in prevalence over the last few decades [1]
To evaluate the impact of GOS/inulin supplementation on the microbiota of pregnant mice, stools were collected on day 0 before GOS/inulin supplementation (D0) and on day 18 corresponding to the end of gestation (D18P)
To evaluate the functional impact of these changes in fecal microbiota, shortchain fatty acids (SCFAs) concentrations were measured by gas chromatography
Summary
Food allergy (FA) is a common non-communicable disease that affects up to 10% of infants in some countries and has been increasing in prevalence over the last few decades [1]. FA is characterized by a failure of oral tolerance induction and by a predominantly T helper (Th) 2-skewed immune dysregulation, regulatory T cells (Treg) dysfunction, and the secretion of antigen-specific immunoglobulin (Ig) E and IgG1 [2, 3]. During allergen-specific immunotherapy, CD4+Foxp3+ Treg development is essential for the establishment of mucosal tolerance suppressing interleukin (IL)-4 production [4,5,6]. CD4+Foxp3+ Treg and CD8+Foxp3+ Treg cooperate to limit allergic symptoms via IL-10 secretion during allergen immunotherapy [7]. Regulatory B cells (Breg) regulate immune responses by suppressing effector T cells through the production of anti-inflammatory cytokines (IL-10 and TGF-b) [8]. IL-10secreting Breg decrease anaphylaxis following a challenge with cow’s milk allergens through the induction of CD4+Foxp3+ Treg [9]
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