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Amelioration of Enterotoxigenic Escherichia coli-induced disruption of intestinal epithelium by Manno-oligosaccharide in weaned pigs
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Abstract
Background: Enterotoxigenic Escherichia coli (ETEC) is one of the major bacterial causes leading to diarrhea and disruption of intestinal epithelium in neonatal animals. Manno-oligosaccharide (MOS) is a prebiotic deprived from natural plants or yeasts. Here, we explored the protective effect of MOS on intestinal epithelium in weaned pigs upon ETEC challenge. Methods: Thirty-two pigs were randomly assigned into four treatments and fed with a basal diet or basal diet containing 0.3% MOS. On day 19, pigs were challenged by ETEC or culture medium. Results: MOS supplementation reduced diarrhea incidence in the pigs upon ETEC challenge (P<0.05). ETEC-challenge elevated the serum concentrations of D-lactate and diamine oxidase (DAO), however, MOS significantly decreased their concentrations in the serum (P<0.05). Moreover, MOS significantly decreased serum concentrations of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in the ETEC-challenged pigs (P<0.05). Interestingly, MOS enhanced the expression and localization of zonula occludens-1 (ZO-1) protein in the duodenal and jejunal epithelium. Moreover, MOS decreased the cell apoptosis rate (P<0.05), but significantly elevated the content of secretory immunoglobulin A (sIgA), glutathione peroxidase (GSH-Px), and superoxide dismutase (SOD) in the jejunal mucosa (P<0.05). Importantly, MOS decreased the expression levels of critical genes involving in mucosal inflammatory responses (TNF-α, IL-1β, TLR4, and NF-κB) and the apoptosis (Caspase 3, Caspase 9, and Bax) in the jejunum upon ETEC challenge (P<0.05). Moreover, MOS up-regulated the expression of mucosa functional genes such as the heme oxygenase-1 (HO-1) and nuclear factor E2-related factor 2 (Nrf2) in the jejunum and ileum (P<0.05), and elevated the expression level of β-defensin 114 (PBD-114) in the duodenum upon ETEC challenge. Conclusions: These results suggested that MOS can alleviate ETEC-induced disruption of intestinal barrier in weaned pigs, which was associated with suppressed inflammation and epithelial cell apoptosis, and improved antioxidant capacity and intestinal barrier functions.
Springer Science and Business Media LLC
Title: Amelioration of Enterotoxigenic Escherichia coli-induced disruption of intestinal epithelium by Manno-oligosaccharide in weaned pigs
Description:
Abstract
Background: Enterotoxigenic Escherichia coli (ETEC) is one of the major bacterial causes leading to diarrhea and disruption of intestinal epithelium in neonatal animals.
Manno-oligosaccharide (MOS) is a prebiotic deprived from natural plants or yeasts.
Here, we explored the protective effect of MOS on intestinal epithelium in weaned pigs upon ETEC challenge.
Methods: Thirty-two pigs were randomly assigned into four treatments and fed with a basal diet or basal diet containing 0.
3% MOS.
On day 19, pigs were challenged by ETEC or culture medium.
Results: MOS supplementation reduced diarrhea incidence in the pigs upon ETEC challenge (P<0.
05).
ETEC-challenge elevated the serum concentrations of D-lactate and diamine oxidase (DAO), however, MOS significantly decreased their concentrations in the serum (P<0.
05).
Moreover, MOS significantly decreased serum concentrations of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in the ETEC-challenged pigs (P<0.
05).
Interestingly, MOS enhanced the expression and localization of zonula occludens-1 (ZO-1) protein in the duodenal and jejunal epithelium.
Moreover, MOS decreased the cell apoptosis rate (P<0.
05), but significantly elevated the content of secretory immunoglobulin A (sIgA), glutathione peroxidase (GSH-Px), and superoxide dismutase (SOD) in the jejunal mucosa (P<0.
05).
Importantly, MOS decreased the expression levels of critical genes involving in mucosal inflammatory responses (TNF-α, IL-1β, TLR4, and NF-κB) and the apoptosis (Caspase 3, Caspase 9, and Bax) in the jejunum upon ETEC challenge (P<0.
05).
Moreover, MOS up-regulated the expression of mucosa functional genes such as the heme oxygenase-1 (HO-1) and nuclear factor E2-related factor 2 (Nrf2) in the jejunum and ileum (P<0.
05), and elevated the expression level of β-defensin 114 (PBD-114) in the duodenum upon ETEC challenge.
Conclusions: These results suggested that MOS can alleviate ETEC-induced disruption of intestinal barrier in weaned pigs, which was associated with suppressed inflammation and epithelial cell apoptosis, and improved antioxidant capacity and intestinal barrier functions.
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