Zhang Hanyun, Gao Jie, He Xiaolong, Gong Zelong, Wan Yu, Hu Tongtong, Li Yubin, Cao Hong
Department of Microbiology, Guangdong Provincial Key Laboratory of Tropical Disease Research, School of Public Health, Southern Medical University, Guangzhou 510515, China.
Nan Fang Yi Ke Da Xue Xue Bao. 2020 Feb 29;40(2):211-218. doi: 10.12122/j.issn.1673-4254.2020.02.12.
To assess the protective effect of the novel postbiotic HM0539 from GG against intestinal infection by enterohemorrhagic O157: H7.
We performed adhesion and invasion experiments to evaluate whether HM0539 could block O157: H7 adhesion to HT-29 cells. The expressions of mucin2 and the tight junction proteins ZO-1 and Occludin in HM0539-treated HT-29 cells were analyzed using immunofluorescence assay and Western blotting. Animal experiments were conducted in mice to observe the survival rate and changes in body weight, intestinal morphology and the intestinal barrier function after the challenge and HM0539 treatment.
HM0539 significantly inhibited the adhesion and invasion of O157: H7 to HT-29 cells in a dose-dependent manner. HM0539 treatment 4 h prior to O157: H7 challenge significantly lowered the adhesion and invasion rates of bacteria as compared with the treatment administered at the same time of challenge ( < 0.05). O157: H7-induced down-regulation of mucin2 and tight junction proteins in HT-29 cells was obviously alleviated by HM0539 treatment of ( < 0.05). In the animal experiment, HM0539 treatment significantly inhibited body weight loss ( < 0.05), alleviated jejunal injury, and inhibited O157: H7-induced destruction of jejunal goblet cells in the challenged mice ( < 0.05). HM0539 also significantly up-regulated the expression of mucin2 and ZO-1 proteins in the jejunum of O157:H7-infected mice ( < 0.05).
HM0539 not only inhibits the adhesion and invasion of O157: H7 to HT-29 cells, but also enhances the resistance against O157: H7 infection in mice by attenuating the destruction of mucin and tight junction proteins.
评估源自嗜热栖热放线菌的新型后生元HM0539对肠出血性O157:H7肠道感染的保护作用。
我们进行了黏附和侵袭实验，以评估HM0539是否能阻断O157:H7对HT-29细胞的黏附。使用免疫荧光分析和蛋白质免疫印迹法分析经HM0539处理的HT-29细胞中黏蛋白2以及紧密连接蛋白ZO-1和闭合蛋白的表达。在小鼠中进行动物实验，观察攻毒和HM0539处理后小鼠的存活率、体重变化、肠道形态以及肠道屏障功能。
HM0539以剂量依赖的方式显著抑制O157:H7对HT-29细胞的黏附和侵袭。在O157:H7攻毒前4小时给予HM0539处理，与在攻毒同时给予处理相比，细菌的黏附和侵袭率显著降低（P<0.05）。HM0539处理明显减轻了O157:H7诱导的HT-29细胞中黏蛋白2和紧密连接蛋白的下调（P<0.05）。在动物实验中，HM0539处理显著抑制体重减轻（P<0.05），减轻空肠损伤，并抑制攻毒小鼠中O157:H7诱导的空肠杯状细胞破坏（P<0.05）。HM0539还显著上调了O157:H7感染小鼠空肠中黏蛋白2和ZO-1蛋白的表达（P<0.05）。
HM0539不仅抑制O157:H7对HT-29细胞的黏附和侵袭，还通过减轻黏蛋白和紧密连接蛋白的破坏来增强小鼠对O157:H7感染的抵抗力。
