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“Background Salmonella enterica is an intracellular facultative ARN-509 mw anaerobe Gram-negative that infects a variety of hosts, which include mammals, avians and reptiles. In human beings, S. enterica causes over 33 million cases of disease worldwide annually, which may vary from gastroenteritis and diarrhea to severe life-threatening systemic disease (typhoid fever) [1]. The outcome of the disease depends on both the serovar of Samonella and the host susceptibility. Salmonella enterica serovar Typhimurium (S. Typhimurium), can infect humans and animals, but Arachidonate 15-lipoxygenase causes different

syndromes in each host. In humans, Salmonella produces enterocolitis, but in mice it causes a systemic illness that resembles human typhoid fever. Because of this, S. Typhimurium is widely used as a model organism to study the host-pathogen interactions that contribute to the onset of the systemic disease [2, 3]. The pathogenic strategy of S. Typhimurium includes penetration of the mucosal barrier, invasion of non-phagocytic cells of the intestinal mucosa and survival and replication inside macrophages of the spleen and liver during the systemic phase. The ability of S. Typhimurium to survive to host defense mechanisms and to cause disease has been directly linked to genes encoded in pathogenicity islands, which are large horizontally acquired regions of the chromosome.