What question did this study set out to answer?

This research aims to explore the impact of RFELNs on intestinal barrier repair and the underlying mechanisms involved in ulcerative colitis.

January 25, 2026Open Access

Robinia pseudoacacia L. Flower Exosome‐Like Nanoparticles (RFELNs) Activate AhR/IL‐22 to Relieve Intestinal Barrier Dysfunction Through Regulating Gut Microbiota‐Interrelated Tryptophan Metabolism in Ulcerative Colitis Mice

Key Points

This research aims to explore the impact of RFELNs on intestinal barrier repair and the underlying mechanisms involved in ulcerative colitis.
Assessed changes in body weight, food intake, DAI score, colon length, and inflammatory levels in mice models.
Evaluated intestinal barrier integrity using permeability analysis, staining, IHC, and western blot assays.
Measured IL-22 expression through immunofluorescent staining and ELISA assay.
Used flow cytometry to analyze ILC3 cell proportions in the colon.
Established an in vitro culture system to investigate RFELNs' mechanisms.
RFELNs improved weight, reduced DAI scores, shortened colon length, and decreased pathological damage in UC mice.
Decreased concentrations of FITC‐dextran and DAO, while enhancing D‐lactate levels.
Increased the number of colonic goblet cells and restored tight junctions.
Enhanced IL-22 expression and the proportions of ILC3 and NCR + ILC3 cells in the colon.
RFELNs activated AhR signaling by increasing indole derivatives from tryptophan metabolism.

Abstract

Background Intestinal barrier dysfunction is a key driver of ulcerative colitis (UC) recurrence and chronic persistence. Modulating group 3 innate lymphoid cells (ILC3) activity and tryptophan‐derived metabolites is crucial for enhancing mucosal repair in UC. Robinia pseudoacacia L. flower exosome‐like nanoparticles (RFELNs) could ameliorate intestinal mucosal injury in mice. This study aimed to investigate the impact of RFELNs on intestinal barrier repair in UC mice and explore the underlying mechanisms. Methods Changes in body weight, food intake, DAI score, colon length, pathological score, and inflammatory factor level were performed to assess the therapeutic effect of RFELNs on DSS‐stimulated UC mouse models. The effects of RFELNs on intestinal barrier integrity were assessed by intestinal barrier permeability analysis, Alcian Blue staining, immunohistochemistry (IHC), and western blot assays. IL‐22 level was measured by immunofluorescent staining and ELISA assay. Besides, flow cytometry was performed to detect the proportions of ILC3 and NCR + ILC3 in the colon. Subsequently, an in vitro culture system consisting of NCM460 cells and MNK3 cells was established to determine potential mechanism of RFELNs’ influence on UC. Results RFELNs prominently relieved pathological symptoms in UC mice, including weight loss, enhanced DAI score, shortened colon, and pathological colon damage. Moreover, RFELNs decreased the concentration of FITC‐dextran and DAO level and enhanced D‐lactate levels. Additionally, RFELNs significantly enhanced the number of colonic goblet cells, restored epithelial tight junctions (TJs), and upregulated TJ protein levels. Moreover, RFELNs enhanced IL‐22 expression and the proportion of ILC3 cells and NCR + ILC3 cells. The protective effect of RFELNs on UC depends on AhR. Further, RFELNs activated AhR pathway by increasing the content of indole derivatives produced by tryptophan metabolism, thus promoting the repair of intestinal barrier damage. Conclusion RFELNs restored intestinal barrier function in UC mice by activating AhR/IL‐22 signaling through regulation of gut microbiota‐dependent tryptophan metabolism.

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