Molecular nutrition & food research · 2018
Lactobacillus acidophilus Alleviated Salmonella-Induced Goblet Cells Loss and Colitis by Notch Pathway.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Wu Haiqin, Ye Lulu, Lu Xiaoxi, Xie Shuang, Yang Qian, Yu Qinghua
Аннотация
SCOPE: The intestinal mucosal barrier, including the mucus layer, protects against invasion of enteropathogens, thereby inhibiting infection. In this study, the protective effect of Lactobacillus on the intestinal barrier against Salmonella infection is investigated. The underlying mechanism of its effect, specifically on the regulation of goblet cells through the Notch pathway, is also elucidated.
METHODS AND RESULTS: Here, the protective effect of Lactobacillus on alleviating changes in the intestinal barrier caused by Salmonella infection is explored. It has been found that Salmonella typhimurium colonizes the colon and damages colonic mucosa. However, Lactobacillus acidophilus ATCC 4356 alleviates the colitis caused by Salmonella infection. Moreover, S. typhimurium infection causes colonic crypt hyperplasia with increased PCNA+ cells, while L. acidophilus administration resolves these pathological changes. In addition, it has been further demonstrated that Salmonella results in severe colitis associated with goblet cells, and Lactobacillus improves colitis similarly associated with goblet cells. Salmonella infection induces goblet cell loss and reduces MUC2 expression by increasing Dll1, Dll4, and HES1 expression, while L. acidophilus reverses epithelial damage by balancing the Notch pathway.
CONCLUSION: The study demonstrates that colitis improvement is controlled by Lactobacillus ATCC 4356 by regulation of the Notch pathway; this finding will be useful for prevention against animal S. typhimurium infection.
METHODS AND RESULTS: Here, the protective effect of Lactobacillus on alleviating changes in the intestinal barrier caused by Salmonella infection is explored. It has been found that Salmonella typhimurium colonizes the colon and damages colonic mucosa. However, Lactobacillus acidophilus ATCC 4356 alleviates the colitis caused by Salmonella infection. Moreover, S. typhimurium infection causes colonic crypt hyperplasia with increased PCNA+ cells, while L. acidophilus administration resolves these pathological changes. In addition, it has been further demonstrated that Salmonella results in severe colitis associated with goblet cells, and Lactobacillus improves colitis similarly associated with goblet cells. Salmonella infection induces goblet cell loss and reduces MUC2 expression by increasing Dll1, Dll4, and HES1 expression, while L. acidophilus reverses epithelial damage by balancing the Notch pathway.
CONCLUSION: The study demonstrates that colitis improvement is controlled by Lactobacillus ATCC 4356 by regulation of the Notch pathway; this finding will be useful for prevention against animal S. typhimurium infection.