PSVIII-26 - Baicalin alleviates lincomycin-induced intestinal injury by regulating gut microbiota in weaned pigs

Abstract: Lincomycin and related antibiotics are widely used in swine clinics, but its side effects including diarrhea and inflammatory bowel disease are difficult to be detected and controlled. The purpose of this study was to investigate the effect and mechanism of baicalin, a flavonoid extracted from scutellaria baicalensis, on alleviating lincomycin-related intestinal injury. Forty-eight 21-day-old weaned pigs were selected and randomly divided into three groups: control group, lincomycin group (LC), and baicalin treatment group (LC + BL). Pigs in the LC and LC + BL groups were administered with 1 g/kg lincomycin in feed for 1 week. In the second week, pigs in the LC + BL group were administered 500 mg/kg baicalin in feed. After 2 weeks, 6 piglets in each group were selected to obtain intestinal samples for subsequent analysis, and the body weight of the remaining piglets was recorded on day 28. The results showed that lincomycin significantly reduced the body weight of the pigs on day 28 (p < 0.05), but baicalin treatment restored the weight of piglets on day 28 to the control level. As for intestinal morphology, lincomycin damaged intestinal morphology and reduced villus height in the jejunum of piglets, but these indexes recovered to the control level after baicalin treatment (p < 0.05). In addition, lincomycin decreased claudin-1, TNF-α, and IL-1β mRNA expression in the jejunum (p < 0.05), but these indexes recovered to the control level after baicalin treatment. Then 16S rDNA sequencing was used to examine the microbial composition in the jejunum. Lincomycin significantly increased the abundance of Proteobacteria, Chloroflexi, and Deinococcota (p < 0.05), but baicalin decreased the abundance of Chloroflexi, Acidobacteriota, Patescibacteria, Myxococcota, and Gemmatimonadota in phylum level (p < 0.05). At genus level, lincomycin significantly increased the abundance of Citrobacter, Corynebacterium, Delftia, Agathobacter, Trichococcus, Tissierellales, Enterococcus, Paracoccus, Shewanella, unclassified_c__Clostridia, Alistipes, Sphingomonas, and Massilia, etc (p < 0.05). However, these results were not observed in the LC + BL group, and baicalin treatment increased the abundance of beneficial bacteria such as norank_f__Muribaculaceae (p < 0.05). Fecal microbiota transplantation was employed to further investigate whether these results were relevant to gut microbes. The body weight, villus height, and crypt depth of mice receiving LC group microbiota were significantly lower than that of the control group, while the body weight of mice receiving LC + BL group microbiota was not significantly different from that of the control group. Overall, these results suggest that baicalin may alleviates lincomycin-induced intestinal damage and inflammation by inhibiting the growth of harmful bacteria. Our findings expand our knowledge of antibiotic-induced injury and provide new avenues for identifying potential therapeutic targets for the treatment of antibiotic-induced injury and its complications.