Fumonisin B1 (FB1), one of the most common mycotoxins contaminating feed and food, has been shown to induce intestinal barrier degradation. However, its role on gut microbiota in this process is still unclear. Alginate oligosaccharides (AOS) have been reported to exert their anti-inflammatory and anti-apoptotic function partially via modulation the gut microbiota. However, little is known about the beneficial effect of AOS on gut microbiota upon FB1 exposure. Results show that FB1 degraded intestinal epithelial barrier function as evidenced by increased pathological epithelial cell shedding, reduced the number of goblet cells, and promoted intestinal cell apoptosis. Markedly, FB1 disturbed the cecal and fecal microbiota composition. FB1 increased the level of Lactobacillus and decreased the relative abundance of beneficial microbes. FB1 largely inhibited the production of short chain fatty acids (SCFAs). AOS greatly ameliorated FB1-induced intestinal damage, inflammation, and oxidative stress (eg., T-SOD and MDA). AOS alleviated gut microbial dysbiosis by promoting the growth of beneficial microbes such as Roseburia, Bifidobacterium, and Akkermansia, and increasing SCFAs production upon FB1 exposure. Moreover, the correlation analysis showed that FB1- and AOS-treated gut microbiota alteration is closely associated with the change of intestinal phenotype. We have thus provided a novel insight into the protective role of AOS on FB1-induced gut microbial dysbiosis.
Keywords: Anti-apoptotic; Anti-inflammatory; Gut dysbiosis; Gut microbiome; Mycotoxin; Prebiotics.
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