ArticleNPJ biofilms and microbiomes2026
Disruption of bile acid homeostasis potentiates Paneth cell ablation by activating the intestinal Farnesoid X receptor in necrotizing enterocolitis.
Article in NPJ biofilms and microbiomes, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Synergistic regulation of gut microbiota and metabolites by breast milk and probiotics in the prevention of neonatal necrotizing enterocolitis: mechanisms and prospects.Translational pediatrics · 2026Review
- Research progress on the role of bile acid metabolism in intestinal epithelial cell injury in necrotizing enterocolitis.Frontiers in pediatrics · 2026Review
- Integrated multi-omics analysis reveals dendritic cell centered regulatory networks and therapeutic targets in necrotizing enterocolitis.Frontiers in immunology · 2026Article
- Intestinal stem cells as innate immune sentinels: coupling environmental sensing to epithelial adaptation.Frontiers in immunology · 2026Review
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7 authors.
Funding
Abstract
Although disrupted bile acid (BA) homeostasis is implicated in necrotizing enterocolitis (NEC), its role in NEC pathogenesis remains unclear. We revealed that secondary BA accumulation in the ileum with severe NEC induced Paneth cell (PC) loss via the activation of the intestinal farnesoid X receptor (FXR). Single-cell RNA sequencing (scRNA-seq) showed that high FXR expression was associated with the differentiation of intestinal stem cells (ISCs) in NEC. Mechanistically, intestinal FXR upregulation induced PC loss by inhibiting Wnt/planar cell polarity (PCP) signaling, which regulates ISC lineage priming toward PCs. Furthermore, disrupting the gut-liver axis by downregulating FGF receptor 4 (FGFR4) abrogated the suppression of the BA synthesis induced by elevated FXR levels in severe NEC, leading to improved outcomes, including a restored Firmicutes/Bacteroidetes ratio and a normalized butyrate concentration. Interestingly, FGFR4 inhibition restored the PC population in a butyrate-dependent manner. Our findings demonstrate that FXR regulated PC generation directly or indirectly via the gut-liver axis.
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