The purpose of this study was to explore the effects of glutamate on piglet growth performance and intestinal immunity function, and to further elucidate its mechanism. In a 2 × 2 factorial design involving immunological challenge (lipopolysaccharide (LPS) or saline) and diet (with or without glutamate), twenty-four piglets were randomly assigned to four groups, each with 6 replicates. Piglets were fed with a basal or glutamate diet for 21 d before being injected intraperitoneally with LPS or saline. Piglet's intestinal samples were collected 4 h after injection. Results showed that glutamate increased daily feed intake, average daily gain, villus length, villus area, and villus length to crypt depth ratio (V/C), and decreased the crypt depth (P < 0.05). Furthermore, glutamate increased the mRNA expression of forkhead box P3 (FOXP3), a signal transducer and activator of transcription 5 (STAT5) and transforming growth factor beta, while decreasing the mRNA expression of RAR-related orphan receptor c and STAT3. Glutamate increased interleukin-10 (IL-10) mRNA expression while decreasing the mRNA expression of IL-1β, IL-6, IL-8, IL-17, IL-21, and tumor necrosis factor-α. At the phylum level, glutamate increased the Actinobacteriota abundance and Firmicutes-to-Bacteroidetes ratio while decreasing Firmicutes abundance. At the genus level, glutamate improved the abundance of beneficial bacteria (e.g., Lactobacillus, Prevotellaceae-NK3B31-group, and UCG-005). Furthermore, glutamate increased the concentrations of short-chain fatty acids (SCFAs). Correlation analysis revealed that the intestinal microbiota is closely related to Th17/Treg balance-related index and SCFAs. Collectively, glutamate can improve piglet growth performance and intestinal immunity by modulating gut microbiota and Th17/Treg balance-related signaling pathways.
Keywords: Glutamate; Growth performance; Intestinal immunity; Intestinal microbiota; Piglets; Th17/Treg balance-related signaling pathways.
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