不同途径下MIMP对炎症性肠病小鼠肠道菌群结构的影响

目的通过葡聚糖硫酸钠诱导小鼠炎症性肠病(IBD)模型并观察不同途经下乳杆菌微小膜蛋白(MIMP)对炎症性肠病小鼠的紧密连接蛋白及菌群结构的影响。方法 C57BL/6小鼠24只根据DSS和MIMP不同干预组合将其分为4组:MIMP腹腔注射组(n=6)、MIMP灌胃组(n=6)、诱导肠炎组(n=6)和健康对照组(n=6),利用Western blot对各组小鼠肠道中紧密连接蛋白(Occludin、JAM-1和ZO-1)的表达进行检测,采用16SrRNA测序技术检测V4区鉴定细菌,并进行菌群差异分析。结果 MIMP腹腔注射及灌胃均可显著提高IBD小鼠肠道中紧密连接蛋白的表达水平,灌胃组效果更为显著;MIMP干预后小鼠肠道中拟杆菌门(Bacteroidetes)丰度增高、厚壁菌门(Firmicutes)及变形菌门(Proteobacteria)丰度降低,LEfSe分析、PCoA分析和PCA分析提示4组小鼠肠道菌群结构差异显著。结论不同途径下MIMP均可显著提高IBD小鼠肠道中紧密连接蛋白的表达水平,改善肠黏膜屏障功能,纠正小鼠肠道菌群结构紊乱。

MIMP in different ways of administration influences the intestinal flora structure ofmice with inflammatory bowel disease

Abstract: Objective To construct the mouse models of inflammatory bowel disease (IBD) with dextran sodium sulfate (DSS) and explore the effect of MIMP in different ways of administration on the intestinal flora structure and tight junction (TJ) protein in mice with IBD. Methods A total of 24 C57BL/6 mice were divided into four groups (n=6), i.e. Intraperitoneal injection group, Gavage group, IBD group, and normal control group. Western blot was used to detect the expression of tight junction proteins (Occludin, JAM-1 and ZO-1) in the intestines of mice in each group, 16S rRNA high throughout pyrosequencing was performed on V4 region to examine the differences in gut microbiota profiles in each group. The obtained data were analyzed using bioinformatics. Results MIMP by intraperitoneal injection and gavage significantly improved the expression level of TJ proteins in the intestinal tracts of IBD mice, with the gavage group superior to the intraperitoneal injection group. After MIMP intervention, the abundance of Bacteroidetes in the intestine increased, and the abundances of Firmicutes and Proteobacteria decreased. LEfSe, PCoA and PCA analyses indicated that the structures of intestinal microbiota in the four groups were significantly different. Conclusion MIMP in different ways of administration can significantly improve the expression level of TJ proteins, improve the function of intestinal mucosa barrier, and correct the structural disorder of intestinal microbiota in the intestinal tract of IBD mice.