Bifidobacterium breve M-16V alleviates cow’s milk allergy by regulating gut microbiota and metabolites in human microbiota-associated mice

Abstract

Cow’s milk allergy (CMA) is one of the most common food allergies, especially in infants and young children. Growing evidence from animal studies has shown that some specific probiotics can alleviate CMA, but clinical evidence remains insufficient due to certain limitations. In the present study, we transplanted fecal material from three CMA children into antibiotic-pretreated mice (hum-CMA mice) to mimic the intestinal microecology of allergic individuals, followed by the allergen sensitization and Bifidobacterium breve (B. breve) M-16V intervention. Our results showed that B. breve M-16V effectively ameliorated CMA symptoms and allergy-related indicators in hum-CMA mice. Moreover, B. breve M-16V differentially affected the composition of intestinal microbes, but consistently, the abundance of beneficial bacteria, such as short-chain fatty acid-producing bacteria, was elevated in all three groups of hum-CMA mice. Subsequent untargeted metabolomics analyses revealed that B. breve M-16V improved the pattern of serum metabolites, and these differential metabolites were mainly involved in glutathione metabolism, glycerophospholipid metabolism, and tryptophan metabolism. All the findings indicate that B. breve M-16V can alleviate the anaphylactic reaction in hum-CMA mice by regulating the intestinal microbiota and metabolites, which provides a valued scientific basis for the clinical application of probiotics in food allergy.

Supplementary files

Article information

Article type
Paper
Submitted
04 May 2025
Accepted
06 Jun 2025
First published
07 Jun 2025

Food Funct., 2025, Accepted Manuscript

Bifidobacterium breve M-16V alleviates cow’s milk allergy by regulating gut microbiota and metabolites in human microbiota-associated mice

H. Shao, F. Min, T. Bai, Y. Liu, S. Zheng, Y. Wu, C. Di, M. Lin, X. Li and H. Chen, Food Funct., 2025, Accepted Manuscript , DOI: 10.1039/D5FO02012C

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