LGG promotes activation of intestinal ILC3 through TLR2 receptor and inhibits salmonella typhimurium infection in mice.

Salmonella is a foodborne pathogen that causes disruption of intestinal mucosal immunity, leading to acute gastroenteritis in the host. In this study, we found that Salmonella Typhimurium ( STM ) infection of the intestinal tract of mice led to a significant increase in the proportion of Lacticaseibacillus , while the secretion of IL-22 from type 3 innate lymphoid cells (ILC3) increased significantly. Feeding Lacticaseibacillus rhamnosus GG ( LGG ) effectively alleviated the infection of STM in the mouse intestines. TLR2 -/- mice experiments found 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 inhibiting STM infection.