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<i>Salmonella enterica</i> serovar Infantis (<i>S.</i> Infantis) is an intracellular bacterial pathogen. It is prevalent but resistant to antibiotics. Therefore, the therapeutic effect of antibiotics on <i>Salmonella</i> infection is limited. In this study, we used the piglet diarrhea model and the Caco2 cell model to explore the mechanism of probiotic <i>Lactobacillus johnsonii</i> L531 (<i>L. johnsonii</i> L531) against <i>S.</i> Infantis infection. <i>L. johnsonii</i> L531 attenuated <i>S.</i> Infantis-induced intestinal structural and cellular ultrastructural damage. The expression of NOD pathway-related proteins (NOD1/2, RIP2), autophagy-related key proteins (ATG16L1, IRGM), and endoplasmic reticulum (ER) stress markers (GRP78, IRE1) were increased after <i>S.</i> Infantis infection. Notably, <i>L. johnsonii</i> L531 pretreatment not only inhibited the activation of the above signaling pathways but also played an anti-<i>S.</i> Infantis infection role in accelerating autophagic degradation. However, RIP2 knockdown did not interfere with ER stress and the activation of autophagy induced by <i>S.</i> Infantis in Caco2 cells. Our data suggest that <i>L. johnsonii</i> L531 pretreatment alleviates the intestinal damage caused by <i>S.</i> Infantis by inhibiting NOD activation and regulating ER stress, as well as promoting autophagic degradation.