Disorders of the small intestinal microenvironment in ovalbumin-sensitized mice and mitigation strategies of 2 ′-fucosyllactose and Bifidobacterium longum subsp. Infantis

The small intestine is responsible for approximately 90% of nutrient absorption, and it is widely believed that food allergens primarily sensitize through the small intestine. No study to date has investigated the association between food allergy (FA) and the altered small intestinal microenvironment (SIM), which would help to understand the biological process linking FA, and could provide new insights into the nutritional modulation of FA. In this study, we aimed to investigate the association between the development of FA and the altered SIM in ovalbumin-sensitized mice, as well as elucidate the underlying mechanisms by which Bifidobacterium longum subsp. Infantis ( B. infantis ) and/or 2 ' -fucosyllactose regulate allergenic reactions from the perspective of SIM. Our findings demonstrate that ovalbumin-induced disruption of SIM is characterized by increased bacteria diversity, dysregulated production of organic acids and amino acids, elevated ileal pH levels, and disrupted intestinal tight junctions. Furthermore, B. infantis and 2 ' -fucosyllactose cotreatment most significantly repaired ovalbumin sensitization-induced SIM dysbiosis compared to mono-treatment with either B. infantis or 2 ' -fucosyllactose alone. Additionally, impaired intestinal barrier function may impact lung homeostasis by influencing material exchange between the lumen and tissues, thereby increasing susceptibility to pulmonary. Notably, B. infantis and/or 2 ' -fucosyllactose differentially regulated both SIM and lung homeostasis. The present study supports the notion that disrupted small intestinal microenvironment homeostasis underlie the development of food allergy and highlights the significance of the small intestine-lung axis as a target for probiotic and/or prebiotic-mediated modulation of food allergy.