Key Laboratory of Dairy Science, Ministry of Education, College of Food Science and Engineering, Northeast Agricultural University, Harbin 150030, China.
Key Laboratory of Dairy Science, Ministry of Education, College of Food Science and Engineering, Northeast Agricultural University, Harbin 150030, China.
Food Res Int. 2024 Dec;197(Pt 1):115235. doi: 10.1016/j.foodres.2024.115235. Epub 2024 Oct 21.
Ulcerative colitis (UC) is an immune-mediated intestinal disease without a comprehensive cure, and the alleviation of UC has become an urgent problem. The results showed that JY062 with its EPS group (JEC) alleviated the intestinal barrier damage caused by LPS. After JEC intervention on Caco-2 cells, resulted in upregulation of ZO-1, Claudin-1, Occludin and MUC2 transcript levels and decreased mRNA expression of Claudin-2 (p < 0.05). JEC effectively attenuated the inflammatory response in UC mice and restoration of immunoglobulin levels (IgG, IgM and IgA), which resulted in shortening and swelling of the colon, disappearance of goblet cells, infiltration of inflammatory cells and mucosal damage were alleviated in mice. Similarly, changes in the expression of MUC2 and tight junction proteins after JEC intervention also occurred in UC mice. Administration of JEC significantly inhibited the differentiation of pro-inflammatory Th17 cells in the thymus and peripheral blood, promoted the differentiation of CD4+ T cells to Treg cells, and effectively regulated DSS-induced macrophage imbalance, which was manifested by the polarization of pro-inflammatory M1 macrophages to anti-inflammatory M2 macrophages. This study clearly demonstrates that JEC could significantly prevent intestinal barrier on DSS-induced experimental colitis and could be applied as a potential symbiotic strategy to assist in the alleviation of UC.
溃疡性结肠炎(UC)是一种免疫介导的肠道疾病,目前尚无根治方法,缓解 UC 已成为当务之急。结果表明,JY062 及其 EPS 组(JEC)缓解了 LPS 引起的肠道屏障损伤。JEC 干预 Caco-2 细胞后,ZO-1、Claudin-1、Occludin 和 MUC2 的转录水平上调,Claudin-2 的 mRNA 表达下调(p<0.05)。JEC 能有效减轻 UC 小鼠的炎症反应,恢复免疫球蛋白水平(IgG、IgM 和 IgA),从而减轻结肠缩短和肿胀、杯状细胞消失、炎症细胞浸润和黏膜损伤。同样,JEC 干预后 UC 小鼠 MUC2 和紧密连接蛋白的表达也发生了变化。JEC 给药可显著抑制胸腺和外周血中促炎 Th17 细胞的分化,促进 CD4+T 细胞向 Treg 细胞的分化,并有效调节 DSS 诱导的巨噬细胞失衡,表现为促炎 M1 巨噬细胞向抗炎 M2 巨噬细胞的极化。本研究明确表明,JEC 可显著预防 DSS 诱导的实验性结肠炎中的肠道屏障损伤,可作为一种潜在的共生策略,辅助缓解 UC。