Lactobacillus rhamnosus GG Reduces β-conglycinin- Allergy-Induced Apoptotic Cells by Regulating Bacteroides and Bile Secretion Pathway in Intestinal Contents of BALB/c Mice

Allergy can cause intestinal damage, including through cell apoptosis. In this study, intestinal cell apoptosis was first observed in the β-conglycinin (β-CG) allergy model, and the effect of GG (LGG) on reducing apoptosis of cells in the intestine and its underlying mechanisms were further investig...

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Published in:Nutrients Vol. 13; no. 1; p. 55
Main Authors: Chen, Xiaoxu, Wu, Yuekun, Hu, Yaozhong, Zhang, Yan, Wang, Shuo
Format: Journal Article
Language:English
Published: Switzerland MDPI AG 27-12-2020
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Summary:Allergy can cause intestinal damage, including through cell apoptosis. In this study, intestinal cell apoptosis was first observed in the β-conglycinin (β-CG) allergy model, and the effect of GG (LGG) on reducing apoptosis of cells in the intestine and its underlying mechanisms were further investigated. Allergic mice received oral LGG daily, and intestinal tissue apoptotic cells, gut microbiota, and metabolites were evaluated six and nine days after intervention. Terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) analysis revealed that LGG intervention could reduce the incidence of cell apoptosis more effectively than natural recovery (NR). The results of 16S rRNA analysis indicated that LGG intervention led to an increase in the relative abundance of . Metabolite analysis of intestinal contents indicated that histamine, -acetylhistamine, (α)-γ-glutamylhistamine, phenylalanine, tryptophan, arachidonic acid malate, and xanthine were significantly decreased, and deoxycholic acid, lithocholic acid were significantly increased after the LGG intervention on β-CG allergy; the decreases in histamine and (α)-γ-glutamylhistamine were significant compared with those of NR. In conclusion, LGG reduces apoptosis of cells induced by β-CG allergy, which may be related to regulation of and the bile secretion pathway.
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ISSN:2072-6643
2072-6643
DOI:10.3390/nu13010055