LGG Promotes Activation of Intestinal ILC3 through TLR2 Receptor and Inhibits Salmonella Infection in Mice

Abstract Salmonella is a foodborne pathogen that causes disruption of intestinal mucosal immunity, leading to acute gastroenteritis in the host. In this study, it was discovered that infection with Salmonella Typhimurium (STM) results in a significant decrease in the abundance of Lacticaseibacillus in the intestines of mice, while the secretion of IL-22 by ILC3 is significantly increased. Feeding Lacticaseibacillus rhamnosus GG (LGG) effectively alleviated the infection of STM in the mouse intestines. Experiments using TLR2−/− mice revealed that TLR2-expressing dendritic cells (DCs) are crucial for LGG's activation of ILC3. Subsequent in vitro experiments showed that heat-killed LGG (HK-LGG) could promote DCs to secrete IL-23, which in turn further promotes the activation of ILC3 and the secretion of IL-22. Finally, organoid experiments further verified that IL-22 secreted by ILC3 can enhance the intestinal mucosal immune barrier and inhibit STM infection. This study demonstrates that oral administration of LGG is a potential method for preventing STM infection, providing a theoretical basis for the development of new intestinal health modulating products and treatment strategies.