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Effects of glucose oxidase on growth performance, immune function, and intestinal barrier of ducks infected with Escherichia coli O88.

ABSTRACT: The negative effects of dietary antibiotics have become a widespread concern. It is imperative to search for a new type of green, safe, and efficient feed additive that can replace antibiotics. This study was to investigate the effects of glucose oxidase (GOD) on growth performance, immune function, and intestinal barrier in ducks infected with Escherichia coli O88. First, we established the E. coli challenge model of ducks through a preliminary experiment and then carried out the formal experiment by using 144 1-day-old male lean Peking ducklings (50 ± 2.75 g). All ducks were randomly assigned to 1 of 3 dietary treatment groups of basal diet (control), 30 mg/kg virginiamycin (antibiotic), and 200 U/kg GOD (1,000 U/g). Each group consisted of 6 replications with 8 birds per replicate. At day 7, all ducks were orally administered 0.2 mL E coli O88 (3 × 10⁹ cfu/mL) twice, 8 h apart based on the preliminary experiment. The experiment lasted for 28 d. Dietary supplementation with GOD improved growth performance of ducks infected with E. coli. The GOD increased contents of Ig in plasma and secreted Ig A in jejunal mucosa. The GOD group had lower concentrations of inflammatory cytokines (tumor necrosis factor-?, IL-1?, and IL-6) and their upstream regulator Toll-like receptor 4 in the jejunum of ducks than the control group. Supplementation with GOD increased villus height and decreased crypt depth in the jejunum. The gene expression of tight junction proteins (zonula occludens-1, claudin-1 and claudin-2) was enhanced by adding GOD. The GOD decreased intestinal permeability by reducing the concentrations of diamine oxidase and D-lactic in plasma of ducks. There were no significant differences in almost all the indices tested between the GOD and the antibiotic groups. In conclusion, supplementation of GOD improved growth performance, immune function, and intestinal barrier of ducks infected with E. coli O88. Glucose oxidase may serve as a promising alternative therapy to antibiotics to relieve or prevent colibacillosis in ducks.

SUBMITTER: Liu J

PROVIDER: S-EPMC7705042 | biostudies-literature | 2020 Dec

REPOSITORIES: biostudies-literature

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Effects of glucose oxidase on growth performance, immune function, and intestinal barrier of ducks infected with Escherichia coli O88.

Liu Jiao J Liu Guohua G Chen Zhimin Z Zheng Aijuan A Cai Huiyi H Chang Wenhuan W Li Chong C Chen Jiang J Wu Zhengke Z

Poultry science 20200925 12

The negative effects of dietary antibiotics have become a widespread concern. It is imperative to search for a new type of green, safe, and efficient feed additive that can replace antibiotics. This study was to investigate the effects of glucose oxidase (GOD) on growth performance, immune function, and intestinal barrier in ducks infected with Escherichia coli O88. First, we established the E. coli challenge model of ducks through a preliminary experiment and then carried out the formal experim ...[more]

PMID: 33248570

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Project description:Glucose oxidase (GOD) could benefit intestinal health and growth performance in animals. However, it is unknown whether GOD can protect piglets against bacterial challenge. This study aimed to evaluate the protective effects of GOD on growth performance, clinical symptoms, serum parameters, and intestinal health in piglets challenged by enterotoxigenic Escherichia coli (ETEC). A total of 44 male weaned piglets around 38 days old were divided into four groups (11 replicates/group): negative control (NC), positive control (PC), CS group (PC piglets +40 g/t colistin sulfate), and GOD group (PC piglets +200 g/t GOD). All piglets except those in NC were challenged with ETEC (E. coli K88) on the 11th day of the experiment. Parameter analysis was performed on the 21st day of the experiment. The results showed that the ETEC challenge elevated (p < 0.05) the rectal temperature and fecal score of piglets at certain time-points post-challenge, reduced (p < 0.05) serum glucose and IgG levels but increased (p < 0.05) serum alanine aminotransferase activity, as well as caused (p < 0.05) intestinal morphology impairment and inflammation. Supplemental GOD could replace CS to reverse (p < 0.05) the above changes and tended to increase (p = 0.099) average daily gain during the ETEC challenge. Besides, GOD addition reversed ETEC-induced losses (p < 0.05) in several beneficial bacteria (e.g., Lactobacillus salivarius) along with increases (p < 0.05) in certain harmful bacteria (e.g., Enterobacteriaceae and Escherichia/Shigella). Functional prediction of gut microbiota revealed that ETEC-induced upregulations (p < 0.05) of certain pathogenicity-related pathways (e.g., bacterial invasion of epithelial cells and shigellosis) were blocked by GOD addition, which also normalized the observed downregulations (p < 0.05) of bacterial pathways related to the metabolism of sugars, functional amino acids, nucleobases, and bile acids in challenged piglets. Collectively, GOD could be used as a potential antibiotic alternative to improve growth and serum parameters, as well as attenuate clinical symptoms and intestinal disruption in ETEC-challenged piglets, which could be associated with its ability to mitigate gut microbiota dysbiosis. Our findings provided evidence for the usage of GOD as an approach to restrict ETEC infection in pigs.

Project description:Clostridium butyricum (C. butyricum) is increasingly being used to test the promotion of the gut health of animals. However, the modes of action for such applications for waterfowl remain unclear. Thus, we investigated whether or not intestinal barrier function, immune-related gene expression, and the diversity of the intestinal microbiota in Pekin ducks varied under C. butyricum supplementation. A total of 500 ducks were randomly assigned into five treatments supplemented with basal diets containing: either 0 (group Control), 200 (group CB200), 400 (group CB400) and 600 (group CB600) mg/kg C. butyricum or 150 mg/kg aureomycin (group A150) for 42 days. In comparison with the control group, C. butyricum supplementation enhanced the growth performance and intestinal villus height of Pekin ducks at 42 d. Serum immune indexes and fecal short-chain fatty acids (SCFAs) were all improved at both 21 d and 42 d after C. butyricum addition. The mRNA expression levels of Mucin2, Zonula occludens-1 (ZO-1), Caudin-3, and Occludin increased at 21 d and 42 d and the mRNA expression levels of IL-4 and IL-10 only increased at 42 d after C. butyricum addition. Dietary C. butyricum also resulted in an increase in the number of diversities of operational taxonomic units (OTUs), and an increase in the α-diversity of intestinal microbiota. The addition of C. butyricum altered the composition of the intestinal microbiota from 21 d to 42 d. The relative abundance of Firmicutes and Bacteroidetes showed little changes among groups; however, the relative abundance of Firmicutes/Bacteroidetes were found to have been significantly different between the 21 d and 42 d. C. butyricum administration improved the intestinal health of Pekin ducks by increasing the diversity of intestinal microbiota, enhancing the SCFAs contents, and strengthening the intestinal barrier function and immune systems. The optimal dietary supplementation dosage was recommended as 400 mg/kg in the diet.

Project description:This study was conducted to investigate the influence of zinc (Zn) supplementation on growth performance, intestinal development and intestinal barrier function in Pekin ducks. A total of 480, one-day-old male Pekin ducks were divided into 6 groups with 8 replicates: 0 mg/kg Zn, 0 mg/kg Zn +0.5 mg/kg lipopolysaccharide (LPS), 30 mg/kg Zn, 30 mg/kg Zn +0.5 mg/kg LPS, 120 mg/kg Zn, 120 mg/kg Zn +0.5 mg/kg LPS. The duck primary intestinal epithelial cells (DIECs) were divided into 6 groups: D-Zn (Zinc deficiency, treated with 2 µmol/L zinc Chelator TPEN), A-Zn (Adequate Zinc, basal medium), H-Zn (High level of Zn, supplemented with 20 µmol/L Zn), D-Zn + 20 µg/mL LPS, A-Zn + 20 µg/mL LPS, H-Zn + 20 µg/mL LPS. The results were as follows: in vivo, with Zn supplementation of 120 mg/kg reduced LPS-induced decrease of growth performance and intestine damage (P < 0.05), and increased intestinal digestive enzyme activity of Pekin ducks (P < 0.05). In addition, Zn supplementation also attenuated LPS-induced intestinal epithelium permeability (P < 0.05), inhibited LPS-induced the expression of proinflammatory cytokines and apoptosis-related genes (P < 0.05), as well as reduced LPS-induced the intestinal stem cells mobilization of Pekin ducks (P < 0.05). In vitro, 20 µmol/L Zn inhibited LPS-induced expression of inflammatory factors and apoptosis-related genes (P < 0.05), promoted the expression of cytoprotection-related genes, and attenuated LPS-induced intestinal epithelium permeability in DIECs (P < 0.05). Mechanistically, 20 µmol/L Zn enhanced tight junction protein markers including CLDN-1, OCLD, and ZO-1 both at protein and mRNA levels (P < 0.05), and also increased the level of phosphorylation of TOR protein (P < 0.05) and activated the TOR signaling pathway. In conclusion, Zn improves growth performance, digestive enzyme activity, and intestinal barrier function of Pekin ducks. Importantly, Zn also reverses LPS-induced intestinal barrier damage via enhancing the expression of tight junction proteins and activating the TOR signaling pathway.

Project description:We studied the effect of early pathogenic Escherichia coli infection on newborn calves' intestinal barrier and immune function. A total of 64 newborn Holstein male calves (40-43 kg) were divided into two groups: normal (NG) and test (TG), each with 32 heads. At the beginning of the experiment, the TG calves were orally administered pathogenic E. coli O1 (2.5 × 1011 CFU/mL, 100 mL) to establish a calf diarrhea model. In contrast, the NG calves were given the same amount of normal saline. During the 30 d trial period, the feeding and management of the two groups remained constant. Enzyme-linked immunosorbent assay, quantification PCR, and high-throughput 16S rRNA sequencing technology were used to detect indicators related to the intestinal barrier and immune function in the calf serum and tissues. Pathogenic E. coli O1 had a significant effect on calf diarrhea in the TG; it increased the bovine diamine oxidase (P < 0.05) and endotoxin levels in the serum and decreased (P < 0.05) the intestinal trefoil factor (P < 0.05), Occludin, Claudin-1, and Zonula Occludens 1 (ZO-1) levels in the colon tissue, as well as downregulated the mRNA expression of Occludin, Claudin-1,and ZO-1 in the colon mucosa, leading to increased intestinal permeability and impaired intestinal barrier function. Additionally, pathogenic E. coli had a significant impact on the diversity of colonic microbial flora, increasing the relative abundance of Proteobacteria at the phylum level and decreasing the levels of Firmicutes and Bacteroides. At the genus level, the relative abundance of Escherichia and Shigella in the TG increased significantly (P < 0.05), whereas that of Bacteroides, Butyricicoccus, Rikenellaceae_RC9_gut_group, Blautia, and Lactobacillus was significantly decreased (P < 0.05). In addition, the level of IL-6 in the serum of the TG calves was significantly increased (P < 0.05), whereas the IL-4 and IL-10 levels were significantly decreased (P < 0.05), compared to those in the NG calves. Thus, pathogenic E. coli induced diarrhea early in life disrupts intestinal barrier and impairs immune function in calves.

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Effects of glucose oxidase on growth performance, immune function, and intestinal barrier of ducks infected with Escherichia coli O88.

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Effects of glucose oxidase on growth performance, immune function, and intestinal barrier of ducks infected with Escherichia coli O88.

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