Alleviates -Induced Intestinal Injury in Mice Model by Modulating Inflammation, Apoptosis, and Cecal Microbial-Metabolic Responses.

() is a probiotic known for its ability to enhance host resistance against pathogenic infections. This study aimed to evaluate the protective effects and underlying mechanisms of in a mouse model challenged with (). C57BL/6J mice were pretreated with for 21 days before oral infection with . The probiotic administration significantly prevented infection-induced weight loss and immune organ enlargement. Serum cytokine analysis revealed that increased anti-inflammatory IL-4 and IL-10 levels while reducing pro-inflammatory IL-1β, IL-6, and TNF-α levels. Histological analysis showed that preserved intestinal morphology and inhibited epithelial cell apoptosis. Moreover, the probiotic mitigated the infection-induced decline in volatile fatty acid (VFA) production. 16S rRNA gene sequencing revealed that reshaped the cecal microbiota, characterized by the increased abundance of , , and , and reduced abundance of . Untargeted metabolomic profiling identified differential metabolites-including D-glucono-1,5-lactone, D-erythrose 4-phosphate, and D-sedoheptulose 7-phosphate-enriched in the pentose phosphate pathway, suggesting a regulatory role in redox homeostasis and host response. Collectively, these results indicate that exerts protective effects against infection by modulating inflammation, apoptosis, microbial composition, and metabolic pathways. This work provides new insights into the application of as a functional microbial feed additive in livestock disease prevention.