DK supervised and participated in the sample collection and manus

DK supervised and participated in the sample collection and manuscript

writing. KSJ funded and coordinated the study and contributed to writing the manuscript. All authors have read and approved the final manuscript. KST designed the project, supervised the analyses and interpretation of the molecular phylogenies and Compound C manufacturer participated in writing the manuscript.”
“Background Salmonella enterica is one of the leading causes of food-borne illnesses around the world [1, 2]. There are two major serotypes of Salmonella enterica, namely Salmonella enterica serovar Enteritidis (S. Enteritidis) and Typhimurium (S. Typhimurium). In recent years, S. Enteritidis represents one of the most commonly reported selleck chemical serotypes associated with food poisoning illness in the United States [3]. Two hallmarks of Salmonella pathogenesis are the Cisplatin clinical trial invasion of non-phagocytic cells such

as the epithelial cells of the intestinal mucosa, and the survival inside macrophages during systemic infection. The mechanisms of both processes are linked to the functions of two type III secretion systems (T3SS) of Salmonella that are encoded and regulated by a cluster of genes at the Salmonella Pathogenicity Island 1 and 2 (SPI-1 and SPI-2), respectively. It is believed that SPI-1 T3SS is responsible for invasion of non-phagocytic cells, while SPI-2 T3SS is essential for intracellular replication and systemic infection [4, 5]. In order to survive and replicate in an aerobic environment, organisms including Salmonella

must cope with reactive oxygen species such as hydrogen peroxide (H2O2), which are formed in respiring cells as incomplete Diflunisal reduction products of molecular oxygen, and which can cause damage to DNA, RNA, protein, and lipids [6–8]. To respond to oxidative stress, bacteria activate a set of globally regulated genes, including two known stimulons: peroxide stimulons and superoxide stimulons [7, 9–12]. The response of Salmonella to oxidative stress represents a key component of its pathogenesis [7, 9]. Reactive oxygen species generated by the NADPH phagocytic oxidase system in phagocytes play an important role in controlling Salmonella replication in macrophages and systemic infection in the spleen [13, 14]. To combat the damaging effects of this oxidative stress and survive in macrophages during systemic infection such as in the spleen, it is believed that Salmonella uses unique strategies and expresses specific proteins to carry out defense and repair functions [7, 9]. While little is known about the expression of SPI-1 factors upon oxidative stress, several SPI-1 factors SipA, SopA, SopB, SopD, and SopE2 of S. Typhimurium were found to be expressed in the spleen of infected animals at the late stages of infection when Salmonella is believed to replicate in splenic macrophages [15, 16].

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