Amelioration of enterotoxigenic Escherichia coli-induced disruption of intestinal epithelium by manno-oligosaccharide in weaned pigs. (July 2021)

• Record Type: Journal Article
• Authors: Yu, En; Chen, Daiwen; Yu, Bing; Luo, Yuheng; Zheng, Ping; Yin, Heng; Mao, Xiangbing; Huang, Zhiqing; Yu, Jie; Luo, Junqiu; HuiYan, ; He, Jun
• Is Part Of: Journal of functional foods. Volume 82(2021)
• Publication Date: 2021-07
• Subjects: Manno-oligosaccharide -- Weaned pigs -- Intestinal barrier -- Inflammation response -- Apoptosis; CMOS pigs were fed with basal diet containing 3 g/kg MOS product -- CON pigs were fed with a basal diet -- ECON pigs were fed with a basal diet and challenged by ETEC -- EMOS pigs were fed with basal diet containing 3 g/kg MOS product and challenged by ETEC -- ETEC Enterotoxigenic Escherichia coli -- Nrf2 nuclear factor erythroid-derived 2-related factor 2 -- DAO diamine oxidase -- HO-1 heme oxygenase-1 -- BAX B-cell lymphoma-2-associated X protein -- BCL-2 B-cell lymphoma-2 -- cysteinyl aspartate-specific proteinase-3 (caspase-3) caspase-8 and caspase-9, Porcine β-defensin (PBD)114 and PBD129 -- Zo-1 zonula occludens-1; Functional foods -- Analysis -- Periodicals; Food -- Biotechnology -- Periodicals; Nutrition -- Periodicals; 613.2
• DOI: 10.1016/j.jff.2021.104492
• Languages: English
• ISSNs: 1756-4646

Abstract

Highlights: MOS is a natural prebiotic that can alleviate ETEC-induced diarrhea. MOS alleviates ETEC-induced intestinal epithelium disruption. MOS elevated antioxidant capacity in the intestinal mucosa. MOS decreases the expression levels of apoptosis-related genes. Abstract: To explored the protective effect of manno -oligosaccharides (MOS) on intestinal epithelium exposure to Enterotoxigenic Escherichia coli (ETEC), thirty-two pigs were assigned into four treatments and fed with basal or MOS-containing (0.3% MOS) diet. Pigs were challenged by ETEC or culture medium. Results show that MOS not only reduced diarrhea incidence and fecal E. coli abundance but decreased serum D-lactate and DAO concentrations upon ETEC-challenge ( P < 0.05). Interestingly, MOS attenuated ETEC-induced intestinal injury, as indicated by improved mucosa morphology and tight-junction protein distribution and decreased cell apoptosis. MOS also increased sIgA, GSH-Px, and SOD contents in jejunum ( P < 0.05). Importantly, MOS down-regulated genes involved in inflammatory responses (TNF-α, IL-1β, TLR4, and NF-κB) and apoptosis (Caspase 3, Caspase 9, and Bax), but up-regulated expressions of antioxidant genes (HO-1 and Nrf2) ( P < 0.05). These results suggested that MOS can alleviate ETEC-induced intestinal injury, which was associated with suppressed inflammation and improved antioxidant capacity and intestinal epithelial functions.