The intestinal health of broilers is closely related to their overall health status, as the intestinal tract serves not only as a site for nutrient digestion and absorption but also as the body's first line of defense against external pathogens. Salmonella typhimurium (S.Tm) infection primarily affects the intestines of chicks, leading to intestinal dysplasia, enteritis, and septicemia (Lihong Wang et al., 2018).

Salmonella enteritis in poultry can result in reduced immune function, decreased growth rate, and increased mortality. The main methods for preventing and controlling salmonella-induced enteritis in chicks include antibiotics, probiotics, and other biological agents (Wu et al., 2023). However, biologics only have a better adjuvant therapeutic effect when the environment is controlled and the health condition is good. Therefore, it is of great significance to establish prevention and control measures for salmonella-induced enteritis in the post-antibiotic era from the perspective of nutritional immunity to ensure the health of chicks.

The role of S.Tm infection in intestinal pathology is particularly significant. Berkes (Berkes et al., 2003) reported that the enteropathogenic bacterium S.Tm is associated with the disruption of tight junctions in intestinal epithelial tissue. S.Tm disrupts tight junctions by interfering with specific proteins and causing disturbances (Matsuzawa et al., 2005). The molecules involved in decision-making in Salmonella enteritis can also serve as key nodes in immune signaling. Additionally, increased permeability manifests the loss of intestinal epithelial cell integrity during S.Tm infection. Zhang (Zhang et al., 2012) reported that S.Tm infection caused intestinal damage in broilers, which was determined by elevated plasma endotoxin levels. Furthermore, the translocation of S.Tm into the spleen and liver also reflects the disruption of the intestinal epithelial barrier by S.Tm. Li (Li et al., 2017) also found that S.Tm severely damaged the intestinal structure of mice, resulting in an increased translocation of bacteria into mesenteric lymph nodes. These results suggest that S.Tm infection can disrupt both host's intestinal permeability and intestinal immunity.