Search

This study was to investigate the effects of chitosan-chelated zinc on ileal microbiota, inflammatory response, and barrier function in weaned piglets challenged with Escherichia coli K88. Piglets of the chitosan-chelated zinc treatment (Cs-Zn; 100 mg zinc + 766 mg chitosan/kg basal diet, from chitosan-chelated zinc) and the chitosan treatment (CS, 766 mg chitosan/kg basal diet) had significantly increased ileal villus height and the ratio of villi height to crypt depth. CS-Zn group piglets had a higher abundance of Lactobacillus in the ileal digesta, while the abundance of Streptococcus, Escherichia shigella, Actinobacillus, and Clostridium sensu stricto 6 was significantly decreased. The concentrations of propionate, butyrate, and lactate in the CS-Zn group piglets were significantly increased, while the pH value was significantly decreased. Furthermore, the concentrations of IL-1β, TNF-α, MPO, and INF-γ in the ileal mucosa of the CS-Zn and the H-ZnO group (pharmacological dose of 1600 mg Zn/kg basal diet, from ZnO) were significantly lower than those of the control group fed with basal diet, and the mRNA expression of TLR4, MyD88, and NF-κB of the CS-Zn group was also reduced. In addition, the mRNA expression of IGF-1 was increased, the protein expression of occludin and claudin-1 was enhanced, while the mRNA expression of caspase 3 and caspase 8 was decreased in the CS-Zn group. These results suggest CS-Zn treatment could help modulate the composition of ileal microbiota, attenuate inflammatory response, and maintain the intestinal function in weaned piglets challenged with Escherichia coli K88. • Chitosan-chelated zinc significantly modulated ileal microbiota. • Chitosan-chelated zinc can improve ileal health. • The ileal microbiota plays an important role in host health.

The present study was conducted to test the hypothesis that dietary supplementation with a nano chitosan–zinc complex (CP–Zn, 100 mg/kg Zn) could alleviate weaning stress in piglets challenged with enterotoxigenic Escherichia coli K88 by improving growth performance and intestinal antioxidant capacity. The in vivo effects of CP–Zn on growth performance variables (including gastrointestinal digestion and absorption functions and the levels of key proteins related to muscle growth) and the antioxidant capacity of the small intestine (SI) were evaluated in seventy-two weaned piglets. The porcine jejunal epithelial cell line IPEC-J2 was used to further investigate the antioxidant mechanism of CP–Zn in vitro. The results showed that CP–Zn supplementation increased the jejunal villus height and decreased the diarrhoea rate in weaned piglets. CP–Zn supplementation also improved growth performance (average daily gain and average daily feed intake), increased the activity of carbohydrate digestion-related enzymes (amylase, maltase, sucrase and lactase) and the mRNA expression levels of nutrient transporters (Na+-dependent glucose transporter 1, glucose transporter type 2, peptide transporter 1 and excitatory amino acid carrier 1) in the jejunum and up-regulated the expression levels of mammalian target of rapamycin (mTOR) pathway-related proteins (insulin receptor substrate 1, phospho-mTOR and phospho-p70S6K) in muscle. In addition, CP–Zn supplementation increased glutathione content, enhanced total superoxide dismutase (T-SOD) and glutathione peroxidase (GSH-px) activity, and reduced malondialdehyde (MDA) content in the jejunum. Furthermore, CP–Zn decreased the content of MDA and reactive oxygen species, enhanced the activity of T-SOD and GSH-px and up-regulated the expression levels of nuclear factor erythroid 2-related factor 2 (Nrf2) pathway-related proteins (Nrf2, NAD(P)H:quinone oxidoreductase 1 and haeme oxygenase 1) in lipopolysaccharide-stimulated IPEC-J2 cells. Collectively, these findings indicate that CP–Zn supplementation can improve growth performance and the antioxidant capacity of the SI in piglets, thus alleviating weaning stress.

Escherichia coli (E. coli) infection is very common among young growing animals, and zinc supplementation is often used to alleviate inflammation induced by this disease. Therefore, the objective of this study was to evaluate whether chitosan-chelated zinc (CS-Zn) supplementation could attenuate gut injury induced by E. coli challenge and to explore how CS-Zn modulates cecal microbiota and alleviates intestinal inflammation in weaned rats challenged with E. coli. 36 weaned rats (55.65 ± 2.18 g of BW, n = 12) were divided into three treatment groups consisting of unchallenged rats fed a basal diet (Control) and two groups of rats challenged with E. coli and fed a basal diet or a diet containing 640 mg/kg CS-Zn (E. coli + CS-Zn, containing 50 mg/kg Zn) for a 14-day experiment. On days 10 to 12, each rat was given 4 ml of E. coli solution with a total bacteria count of 1010 CFU by oral gavage daily or normal saline of equal dosage. CS-Zn supplementation mitigated intestinal morphology impairment (e.g. higher crypt depth and lower macroscopic damage index) induced by E. coli challenge (P < 0.05), and alleviated the increase of Myeloperoxidase (MPO) activity after E. coli challenge (P < 0.05). 16S rRNA sequencing analyses revealed that E. coli challenge significantly increased the abundance of Verrucomicrobia and E. coli (P < 0.05). However, CS-Zn supplementation increased the abundance of Lactobacillus and decreased the relative abundance of Proteobacteria, Desulfovibrio and E. coli (P < 0.05). The concentrations of butyrate in the cecal digesta, which decreased due to the challenge, were higher in the E. coli + CS-Zn group (P < 0.05). In addition, CS-Zn supplementation significantly prevented the elevation of pro-inflammatory cytokines IL-6 concentration and up-regulated the level of anti-inflammatory cytokines IL-10 in cecal mucosa induced by E. coli infection (P < 0.05). In conclusion, these results indicate that CS-Zn produces beneficial effects in alleviating gut mucosal injury of E. coli challenged rats by enhancing the intestinal morphology and modulating cecal bacterial composition, as well as attenuating inflammatory response.

The aim of this work was to study the role of hepatic metabolism of compensatory growth in piglets induced by protein restriction and subsequent protein realimentation. Thirty-six weaned piglets were randomly distributed in a control group and a treatment group. The control group piglets were fed with a normal protein level diet (18.83% CP) for the entire experimental period (day 1-28). The treatment group piglets were fed with a protein-restriction diet (13.05% CP) for day 1 to day 14, and the diet was restored to normal protein level diet for day 15 to day 28. RNA-seq is used to analyze samples of liver metabolism on day 14 and day 28, respectively. Hepatic RNA-sequencing analysis revealed that some KEGG signaling pathways involved in glycolipid metabolism (eg, "AMPK signaling pathway," "insulin signaling pathway," and "glycolysis or gluconeogenesis") were significantly enriched on day 14 and day 28. On day 14, protein restriction promoted hepatic lipogenesis by increasing the genes expression level of ACACA, FASN, GAPM, and SREBP1C, decreasing protein phosphorylation levels of AMPKɑ and ACC in AMPK signaling pathway. In contrast, on day 28, protein realimentation promoted hepatic gluconeogenesis by increasing the concentration of G6Pase and PEPCK, decreasing protein phosphorylation levels of IRS1, Akt, and FoXO1 in insulin signaling pathway. In addition, protein realimentation activated the GH-IGF1 axis between the liver and skeletal muscle. Overall, these findings revealed the importance of liver metabolism in achieving compensatory growth.