Abstract:Salmonellosis is one of the most widespread food-borne diseases throughout the world, not only causes economic losses to the breeding industry, but also poses a threat to human health. Avian Salmonella enters the small intestine where infection can be established, inducing intestinal epithelial cells express a number of TLRs and inflammation. These lead to the expression of chemokines that attract immune effector cells to the sites of infection. Following translocation across the intestinal epithelial barrier, bacteria are phagocytosed by cells such as macrophages and DCs, macrophages are its preferred cell type. The adaptive immune response is stimulated by the innate immune system through antigen presentation to lymphocytes. Adaptive immunity can clear infection within 2-3 weeks following infection by a Th1 dominated response in the gut and deeper tissues. In contrast, avian systemic salmonellosis caused by the host-adapted serovar S. Pullorum is characterized by invasion from the intestine with multiplication in the spleen, liver and other organs. The stage of infection resulted in little inflammation in vivo or in vitro. S. Pullorum tends to induce an immune response that more closely resembled the Th2 response in mammals and would allow S. Pullorum to establish an intracellular carriage evading Th1-mediated clearance. This review compared the pathogenesis and immune response characteristics of Salmonella, especially the mechanisms by which S. Pullorum evades host immunity and produces the persistent carrier state. Finally, it will be helpful to provide new targets and new opinions for the prevention and control of avian salmonellosis.