MECHANISMS OF GALECTIN 1 INDUCTION BY GALACTOOLIGOSACCHARIDES

Food allergies in infancy have become a growing public health concern. According to the CDC, food allergies are estimated to impact over 8% of children in the US. Galacto-oligosaccharides (GOS), structurally similar to human milk oligosaccharides, modulate the gut microbiota and benefit host health. In an early pilot experiment, GOS feeding resulted in non-statistically significant reductions in peanut-specific IgE, anaphylaxis, intestinal permeability, and increased relative abundance of Akkermansia and Bifidobacterium in peanut-sensitized CC027/GeniUnc mice.Here, we showed in mice and primary human intestinal cells that GOS induced the expression of lgals-1, which encodes Galectin-1 (Gal-1), a glycoprotein with immunomodulatory effects and an established role in suppressing allergic asthma. We first confirmed differential expression of lgals-1 in mice fed GOS compared with control diets by reverse transcription-quantitative (q) PCR. GOS significantly increased lgals-1 expression in the colon of young but not old mice. Computational molecular docking predictions confirmed the binding affinity between GOS and Gal-1, suggesting a direct interaction. We also showed that GOS interacted directly with human primary intestinal cells inducing lgals-1 expression. Additionally, we showed that GOS induced lgals-1 expression in the human intestinal cells by enhancing Bifidobacterium, providing an indirect induction pathway of lgals-1 by GOS. Our study lays the groundwork for mechanistic research exploring a potential prebiotic role in modulating the immune system, specifically for preventing or treating food allergies.