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53. Wilson K: Preparation of genomic DNA from bacteria. Curr Protoc Mol Biol 2001, 00:2.4.1–2.4.5. Competing interests The authors declare they have no competing interests. Authors’ contributions TLW designed the data analysis approach, interpreted results and wrote the manuscript. SH performed the data analysis for Figure  1, Tables  1, 2, 3 and Additional file 1: Table S1, Additional file 2: Table S2 and Additional file 6: Table S4. IA conceived and supervised the study and edited the paper. II supervised the bioinformatics analyses and edited the paper. All authors have read and approved the manuscript.”
“Background Salmonella enterica serovar Typhimurium is an enteroinvasive bacterial

pathogen typically encountered by ingesting contaminated food or water. S. Typhimurium causes self-limiting gastroenteritis in humans and typhoid-like fever in mice [1, 2]. Greater than 99% of the bacteria in murine salmonellosis are killed in the stomach or passed out of the gut [2], but S. Typhimurium that survive passage through the acidic stomach environment enter into the small intestine, where upon they transverse the intestinal epithelial barrier. The bacteria are then phagocytosed by macrophages Selleckchem EPZ015938 or they can actively invade both phagocytic and non-phagocytic cells using a type III secretion system [1]. Following invasion, ZD1839 cost Salmonella disseminates throughout the body leading to a systemic typhoid-like infection [2]. Salmonella forms biofilms on abiotic surfaces such as plastic and egg conveyer belts, which may have a role in environmental survival of this organism [3, 4]. Biofilm formation and aggregation in S. enterica serovar Typhimurium is exemplified by the rdar colony morphology, where colonies grown on media containing Congo red are red, dry, and rough [5, 6]. This morphology requires the production of curli fimbriae and multiple exopolysaccharides [7,

8]. S. Typhimurium also grows enmeshed in EPS rich biofilms on the CRT0066101 surface of gallstones, which may contribute to inefficient antibiotic treatment and facilitates typhoid carriage [9, 10]. Biofilm shedding from colonized gallstones is likely a source of recurring infections [11]. The PhoPQ two-component system is important for intracellular survival within macrophages. Limiting Mg2+, low pH and the presence of antimicrobial peptides are PhoPQ-activating signals in culture [12, 13] but low pH and antimicrobial peptides are important activating signals during intracellular macrophage growth [14]. The PmrAB two component system responds to Fe3+ and low pH, and is activated under Mg2+ limiting conditions by a post-translational mechanism involving PmrD, a PhoPQ-regulated protein.