Abstract

BackgroundShrimp tropomyosin (TM) is a major food allergen that may cause serious allergic responses, lactic acid-producing bacteria (LAPB) are believed to alleviate food allergy, but the mechanisms have not been fully clarified. The aim of this work is to investigate the mechanisms of LAPB in ameliorating food allergy-induced intestinal mucosal disorders and to investigate whether or not these disorders occur by the regulation of gut microbiota and metabolism. MethodsA TM allergy BALB/c mouse model was established, and two LAPB strains, Bifidobacterium longum (Bi) and Bacillus coagulans (Bc), were used for oral treatment in sensitized mice. The allergic mucosal disorders were assessed by histological analysis and ELISAs. Additionally, microbiota and metabolic modifications were determined by 16S rRNA gene amplicon sequencing and GC-TOF-MS, respectively. ResultsYSPB administration suppressed TM-induced intestinal mucosal disorders, restored allergenic Th2 cell over-polarization and dysbiosis, and regulated gut arginine and proline metabolism pathways. Statistical analysis suggested the metabolites aspartate and arginine, as well as several commensal flora groups, to be the critical mediators in the process. ConclusionsThese data demonstrated the correlation between allergic mucosal disorder, T cell subtype differentiation, gut microbiota composition and intestinal metabolism especially the arginine and proline metabolism pathways. We also revealed the significant effects of LAPB in ameliorating food allergy and maintaining the mucosal ecosystem. This study confirmed the efficiency of LAPB in relieving food allergy, provided Bi and Bc as the potential treatment approaches, and suggested amino acid metabolism pathways might be the novel targets for potential clinical applications.

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