Phytomedicine : international journal of phytotherapy and phytopharmacology · 2026
(-)-Epigallocatechin-3-gallate alleviates diarrhea in piglets by suppressing the NMU-NMUR1-ILC2 axis and modulating microbiota-associated energy metabolism.
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Ma Ziwen, Gao Lujia, Hou Wanting, Wu Jiaqi, Wen Xin, Zhang Yahan, Dong Na, Dou Xiujing, Shan Anshan
Аннотация
BACKGROUND: Bacterial diarrhea is considered a global health crisis, accounting for approximately 20 % of deaths related to colorectal cancer. (-)-Epigallocatechin 3-gallate (EGCG), one of the most abundant plant-derived polyphenols in the human diet, has shown promise in managing gastrointestinal disorders. But, the systemic evidence for EGCG in alleviating the progression of diarrhea and the mechanisms involved remain unclear.
OBJECTIVES: This study aims to determine whether EGCG confers diarrhea resistance in piglets under Escherichia coli (E. coli) and what the fundamental mechanisms involved are.
METHODS: Weaned piglets were used to create a E. coli-induced intestinal disorder-diarrhea susceptibility model. Piglets were supplemented with EGCG to identify diarrhea rate and activity of enteric nervous system (ENS). The interaction between the neuromedin U receptor 1 (NMUR1) and typeⅡinnate lymphoid cells (ILC2) was analyzed using RNA sequencing (RNA-seq) and fluorescence colocalization techniques. Metagenomic and metabolomic analyses were further performed to assess the involvement of NMUR1 and the underlying mechanisms of beneficial microbes enriched by EGCG. The effects of beneficial microbes in treating intestinal morphology were investigated through histopathology, Scanning electron microscopy (SEM) and ELISA analysis methods.
RESULTS: EGCG reduced diarrhea rate in piglets by inhibiting the NMU-NMUR1-ILC2 pathway, ameliorating gut microbiota structure, and stimulating intestinal barrier. Apparently, the enteric nerve-microbial axis is linked with EGCG conferring diarrhea resistance in piglets. Mechanistically, EGCG suppressed the NMU-NMUR1-ILC2 axis to reduce the secretion of inflammatory cytokines (TNF-α, IL-6, and IL-8), while concurrently increasing the abundance of beneficial gut microbes and altering signature microbial community functions (energy metabolism pathways); accordingly, EGCG maintained the energy supply balance in gut epithelial cells and promoted the activity of goblet cell and Paneth cell by activating the AMP-activated protein kinase (AMPK)-sirtuin 1 (Sirt1) signaling pathway.
CONCLUSION: EGCG confers diarrhea resistance in E. coli piglets by maintaining intestinal mucosal barrier via the enteric nerve-microbial axis; thus, this study provides a potential prevention strategy for young mammals at risk of diarrhea.
OBJECTIVES: This study aims to determine whether EGCG confers diarrhea resistance in piglets under Escherichia coli (E. coli) and what the fundamental mechanisms involved are.
METHODS: Weaned piglets were used to create a E. coli-induced intestinal disorder-diarrhea susceptibility model. Piglets were supplemented with EGCG to identify diarrhea rate and activity of enteric nervous system (ENS). The interaction between the neuromedin U receptor 1 (NMUR1) and typeⅡinnate lymphoid cells (ILC2) was analyzed using RNA sequencing (RNA-seq) and fluorescence colocalization techniques. Metagenomic and metabolomic analyses were further performed to assess the involvement of NMUR1 and the underlying mechanisms of beneficial microbes enriched by EGCG. The effects of beneficial microbes in treating intestinal morphology were investigated through histopathology, Scanning electron microscopy (SEM) and ELISA analysis methods.
RESULTS: EGCG reduced diarrhea rate in piglets by inhibiting the NMU-NMUR1-ILC2 pathway, ameliorating gut microbiota structure, and stimulating intestinal barrier. Apparently, the enteric nerve-microbial axis is linked with EGCG conferring diarrhea resistance in piglets. Mechanistically, EGCG suppressed the NMU-NMUR1-ILC2 axis to reduce the secretion of inflammatory cytokines (TNF-α, IL-6, and IL-8), while concurrently increasing the abundance of beneficial gut microbes and altering signature microbial community functions (energy metabolism pathways); accordingly, EGCG maintained the energy supply balance in gut epithelial cells and promoted the activity of goblet cell and Paneth cell by activating the AMP-activated protein kinase (AMPK)-sirtuin 1 (Sirt1) signaling pathway.
CONCLUSION: EGCG confers diarrhea resistance in E. coli piglets by maintaining intestinal mucosal barrier via the enteric nerve-microbial axis; thus, this study provides a potential prevention strategy for young mammals at risk of diarrhea.