Key Laboratory of Dairy Science, Ministry of Education, College of Food Science, Northeast Agricultural University, Harbin 150030, China.
Nutrients. 2022 Dec 28;15(1):139. doi: 10.3390/nu15010139.
Ulcerative colitis (UC) is a chronic and recurrent inflammatory bowel disease, and the intestinal barrier is an important line of defense against intestinal disease. Herein, we investigated the effect of JM1 at different doses (1 × 10, 1 × 10, 1 × 10 CFU/day) on colitis mice and explored the possible mechanism. The results showed that JM1 alleviated DSS-induced colitis in mice, with reductions in disease activity index (DAI), histological scores and myeloperoxidase activity as well as alleviation of colonic shortening. Furthermore, JM1 regulated the levels of inflammatory cytokines TNF-α, IL-6, IL-1β, and IL-10; restored the expression of Claudin-3, Occludin, ZO-1, and MUC2; and increased the number of goblet cells and acidic mucin. The 16S rDNA sequencing results indicated that intervention with JM1 balanced the gut microbiota structure by elevating the abundance of beneficial bacteria (, and ) and decreasing that of harmful bacteria ( and ). Meanwhile, the contents of short-chain fatty acids (SCFAs) increased. In conclusion, JM1 could alleviate intestinal barrier damage in colitis mice by modulating the tight junction structures, intestinal mucus layer, inflammatory cytokines, gut microbiota, and SCFAs. It can be considered a potential preventive strategy to alleviate colitis injury.
溃疡性结肠炎（UC）是一种慢性复发性炎症性肠病，肠道屏障是抵御肠道疾病的重要防线。在此，我们研究了不同剂量（1×10、1×10、1×10 CFU/天）的 JM1 对结肠炎小鼠的影响，并探讨了其可能的机制。结果表明，JM1 减轻了 DSS 诱导的结肠炎小鼠的疾病，降低了疾病活动指数（DAI）、组织学评分和髓过氧化物酶活性，同时缓解了结肠缩短。此外，JM1 调节了炎症细胞因子 TNF-α、IL-6、IL-1β 和 IL-10 的水平；恢复 Claudin-3、Occludin、ZO-1 和 MUC2 的表达；增加了杯状细胞和酸性粘蛋白的数量。16S rDNA 测序结果表明，JM1 通过增加有益菌（、和）的丰度和降低有害菌（和）的丰度来平衡肠道微生物群结构。同时，短链脂肪酸（SCFAs）的含量增加。总之，JM1 通过调节紧密连接结构、肠道粘液层、炎症细胞因子、肠道微生物群和 SCFAs 减轻结肠炎小鼠的肠道屏障损伤。它可以被认为是一种缓解结肠炎损伤的潜在预防策略。
