The Prophylactic Protection of Salmonella Typhimurium Infection by Lentilactobacillus buchneri GX0328-6 in Mice

Salmonellosis is a disease caused by non-typhoid Salmonella, and although some lactic acid bacteria strains have been shown previously to relieve Salmonellosis symptoms, little has been studied about the preventive mechanism of Lentilactobacillus buchneri (L. buchneri) against Salmonella infection in vivo. Therefore, the L. buchneri was fed to C57BL/6 mice for 10 days to build a protective system of mice to study its prevention and possible mechanisms. The results showed that L. buchneri GX0328-6 alleviated symptoms caused by Salmonella typhimurium infection among C57BL/6 mice, including low survival rate, weight loss, increase in immune organ index and hepatosplenomegaly, and modulated serum immunoglobulin levels and intrinsic immunity. Importantly, the L. buchneri GX0328-6 enhanced the mucosal barrier of the mouse jejunum by upregulating the expression of tight junction proteins such as ZO-1, occludins, and claudins-4 and improved absorptive capacity by increasing the length of mouse jejunal villus and the ratio of villus length to crypt depth and decreasing the crypt depth. L. buchneri GX0328-6 reduced the intestinal proliferation and invasion of Salmonella typhimurium by modulating the expression of antimicrobial peptides in the intestinal tract of mice, and reduced intestinal inflammation and systemic spread in mice by downregulating the expression of IL-6 and promoting the expression of IL-10. Furthermore, L. buchneri GX0328-6 increased the relative abundance of beneficial bacteria colonies and decreased the relative abundance of harmful bacteria in the cecum microflora by modulating the microflora in the cecum contents.

Automated summary

The preventive mechanism of Lentilactobacillus buchneri (L. buchneri) against Salmonella infection in vivo was studied. L. buchneri alleviated symptoms caused by Salmonella infection, enhanced mucosal barrier, improved absorptive capacity, reduced intestinal inflammation, and modulated gut microbiota.