Preclinical model shows LRS3 reduces allergic responses in food allergy mice, suggesting a novel therapeutic approach.
This study aims to utilize an ovalbumin (OVA)-induced food allergy (FA) mice model to establish the potential relationship by which type III lotus seed resistant starch (LRS3) repairs the intestinal barrier and ameliorates allergic responses through regulating the production of short-chain fatty acids (SCFAs) and the expression of G protein-coupled receptors (GPRs). We found that FA significantly elevated ovalbumin-immunoglobulin E (OVA-IgE) levels in mice to 5085.8 ng mL⁻¹, whereas LRS3 intervention notably reduced OVA-IgE to 3423.72 ng mL⁻¹ and alleviated allergic symptoms. LRS3 increased the contents of propionic acid and butyric acid (p < 0.01) and significantly upregulated the expression of GPRs. In addition, LRS3 promoted intestinal barrier repair, as evidenced by significantly upregulated tight junction protein expression (p < 0.001), improved intestinal permeability, and reduced tissue damage. This study suggests that LRS3 is expected to serve as an effective intervention strategy for the prevention of FA.
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Li et al. (2026) studied this question.
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