Hydrogels are being investigated recently for the bioactive molecules (in particular pharmaceutical proteins) controlled release, such as matrices, and for the living cells encapsulation. Biodegradable nature of hydrogels has created much interest for drug delivery systems. The original three-dimensional structure disintegrates into nontoxic substances to ascertain an excellent biocompatibility of the gel. Chemical cross-linking is the highly resourceful method for the formation of hydrogels having an excellent mechanical strength. Cross-linkers used in hydrogel preparation should be extracted from the hydrogels before use due to their reported toxicity. Physically cross-linked methods for preparation of hydrogel are the alternate solution of cross-linker toxicity.
Background
Intestinal inflammation is prevalent in chicken, which results in decreased growth performance and considerable economic losses. Accumulated findings established the close relationship between gut microbiota and chicken growth performance. However, whether gut microbiota impacts chicken growth performance by lessening intestinal inflammation remains elusive.
Results
Seven-weeks-old male and female chickens with the highest or lowest body weights were significantly different in breast and leg muscle indices and average cross-sectional area of muscle cells. 16S rRNA gene sequencing indicated Gram-positive bacteria, such as Lactobacilli, were the predominant species in high body weight chickens. Conversely, Gram-negative bacteria, such as Comamonas, Acinetobacter, Brucella, Escherichia-Shigella, Thermus, Undibacterium, and Allorhizobium-Neorhizobium-Pararhizobium-Rhizobium were significantly abundant in low body weight chickens. Serum lipopolysaccharide (LPS) level was significantly higher in low body weight chickens (101.58 ± 5.78 ng/mL) compared with high body weight chickens (85.12 ± 4.79 ng/mL). The expression of TLR4, NF-κB, MyD88, and related inflammatory cytokines in the jejunum was significantly upregulated in low body weight chickens, which led to the damage of gut barrier integrity. Furthermore, transferring fecal microbiota from adult chickens with high body weight into 1-day-old chicks reshaped the jejunal microbiota, mitigated inflammatory response, and improved chicken growth performance.
Conclusions
Our findings suggested that jejunal microbiota could affect chicken growth performance by mitigating intestinal inflammation.
It has been established that gut microbiota influences chicken growth performance and fat metabolism. However, whether gut microbiota affects chicken growth performance by regulating fat metabolism remains unclear. Therefore, seven-week-old chickens with high or low body weight were used in the present study. There were significant differences in body weight, breast and leg muscle indices, and cross-sectional area of muscle cells, suggesting different growth performance. The relative abundance of gut microbiota in the caecal contents at the genus level was compared by 16S rRNA gene sequencing. The results of LEfSe indicated that high body weight chickens contained Microbacterium and Sphingomonas more abundantly (P < 0.05). In contrast, low body weight chickens contained Slackia more abundantly (P < 0.05). The results of H & E, qPCR, IHC, WB and blood analysis suggested significantly different fat metabolism level in serum, liver, abdominal adipose, breast and leg muscles between high and low body weight chickens. Spearman correlation analysis revealed that fat metabolism positively correlated with the relative abundance of Microbacterium and Sphingomonas while negatively correlated with the abundance of Slackia. Furthermore, faecal microbiota transplantation was performed, which verified that transferring faecal microbiota from adult chickens with high body weight into oneday-old chickens improved growth performance and fat metabolism in liver by remodelling the gut microbiota. Overall, these results suggested that gut microbiota could affect chicken growth performance by regulating fat metabolism.
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