Taraxacum-derived extracellular nanovesicles attenuate dss-induced colitis through coordinated modulation of gut microbiota, intestinal barrier, and mucosal inflammation

结肠炎 溃疡性结肠炎 炎症性肠病 炎症 免疫学 细胞外 细胞因子 肠粘膜 肠道菌群 化学 免疫系统 医学 右旋糖酐 中性粒细胞胞外陷阱 转录组 巨噬细胞 促炎细胞因子 免疫荧光 免疫 紧密连接 病理 下调和上调 显微镜下结肠炎 胃肠道 病态的 脂质运载蛋白
作者
Zilong Lun,Yanan Han,Nan Li,Shiying Li,Wei Liu,Chun Yang,Yan Zhang
出处
期刊:Journal of Nanobiotechnology [BioMed Central]
标识
DOI:10.1186/s12951-026-04920-2
摘要

Abstract Background Ulcerative colitis (UC) is a chronic inflammatory disease of the colon associated with dysregulated mucosal immunity and gut microbiota imbalance. Safe and effective long-term treatment options remain limited. In this study, we isolated Taraxacum-derived extracellular nanovesicles (TENVs) and evaluated their effects in a dextran sulfate sodium (DSS)-induced colitis model. Methods Colitis was induced in mice with 3% DSS. The therapeutic effects of TENVs were evaluated using histopathology, inflammatory cytokine profiling, intestinal barrier assessment, and immunofluorescence (IF) analysis. Potential mechanisms were investigated by RNA-seq, Western blotting, 16S rDNA sequencing, and fecal microbiota transplantation (FMT). Results TENVs showed typical nanovesicular morphology and remained stable in simulated gastric and intestinal fluids. Oral treatment with TENVs markedly attenuated DSS-induced colitis. Mice showed improved clinical indices, less histological damage, and better-preserved epithelial barrier integrity, together with reduced macrophage activation, colonic MPO and IL-17A expression, and circulating pro-inflammatory cytokines. Transcriptomic profiling and immunoblotting revealed changes consistent with attenuation of IL-17/MAPK-associated inflammatory signaling. TENVs also reshaped the gut microbiota. FMT from donors receiving TENVs alleviated colitis in recipient mice. Conclusion TENVs act on multiple pathological processes in DSS-induced colitis. Their combined effects on mucosal inflammation, epithelial barrier integrity, IL-17/MAPK-associated inflammatory signaling, and the gut microbiota may jointly contribute to the observed protection.
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