b Percent relative to the wild-type (WT). Figure 4 Comparison of the WT and the arcA mutant for surface appendages and flagella via microscopy. Scanning electron microscopy (SEM) was used to evaluate the WT (A) and the arcA mutant (C) for the presence/absence of surface appendages and negative staining followed by transmission electron microscopy (TEM) was used to evaluate the WT (B) and the arcA mutant (D) for the

presence/absence of flagella. Cells {Selleck Anti-infection Compound Library|Selleck Antiinfection Compound Library|Selleck Anti-infection Compound Library|Selleck Antiinfection Compound Library|Selleckchem Anti-infection Compound Library|Selleckchem Antiinfection Compound Library|Selleckchem Anti-infection Compound Library|Selleckchem Antiinfection Compound Library|Anti-infection Compound Library|Antiinfection Compound Library|Anti-infection Compound Library|Antiinfection Compound Library|Anti-infection Compound Library|Antiinfection Compound Library|Anti-infection Compound Library|Antiinfection Compound Library|Anti-infection Compound Library|Antiinfection Compound Library|Anti-infection Compound Library|Antiinfection Compound Library|Anti-infection Compound Library|Antiinfection Compound Library|Anti-infection Compound Library|Antiinfection Compound Library|Anti-infection Compound Library|Antiinfection Compound Library|buy Anti-infection Compound Library|Anti-infection Compound Library ic50|Anti-infection Compound Library price|Anti-infection Compound Library cost|Anti-infection Compound Library solubility dmso|Anti-infection Compound Library purchase|Anti-infection Compound Library manufacturer|Anti-infection Compound Library research buy|Anti-infection Compound Library order|Anti-infection Compound Library mouse|Anti-infection Compound Library chemical structure|Anti-infection Compound Library mw|Anti-infection Compound Library molecular weight|Anti-infection Compound Library datasheet|Anti-infection Compound Library supplier|Anti-infection Compound Library in vitro|Anti-infection Compound Library cell line|Anti-infection Compound Library concentration|Anti-infection Compound Library nmr|Anti-infection Compound Library in vivo|Anti-infection Compound Library clinical trial|Anti-infection Compound Library cell assay|Anti-infection Compound Library screening|Anti-infection Compound Library high throughput|buy Antiinfection Compound Library|Antiinfection Compound Library ic50|Antiinfection Compound Library price|Antiinfection Compound Library cost|Antiinfection Compound Library solubility dmso|Antiinfection Compound Library purchase|Antiinfection Compound Library manufacturer|Antiinfection Compound Library research buy|Antiinfection Compound Library order|Antiinfection Compound Library chemical structure|Antiinfection Compound Library datasheet|Antiinfection Compound Library supplier|Antiinfection Compound Library in vitro|Antiinfection Compound Library cell line|Antiinfection Compound Library concentration|Antiinfection Compound Library clinical trial|Antiinfection Compound Library cell assay|Antiinfection Compound Library screening|Antiinfection Compound Library high throughput|Anti-infection Compound high throughput screening| were grown anaerobically in LB-MOPS-X media and the samples were prepared as described in Materials and Methods. b. Virulence in mice The microarray data (Additional file 1: Table S1) showed that ArcA does not significantly regulate the transcription of the virulence genes found in SPI-1, which are important for the ability of Salmonella to invade host epithelial cells [2, 3, 45–47]. However, few virulence genes related to SPI-2 (sspH2) and SPI-3 (mgtCB, slsA, STM3784) were affected by ArcA. Therefore, to evaluate these findings, we tested the virulence of the arcA mutant in a murine model of mucosal and acute infection using immunocompetent C57BL/6 mice. The arcA mutant was as virulent as LBH589 price the WT strain when 250 CFU/mouse were inoculated via i.p. (Figure 5A). Since intramacrophage survival and replication of Salmonella permits the colonization of the spleen and liver of mice [4, 48], a further virulence comparison of the WT and the arcA mutant was performed

using a mixed infection assay. The data showed that the arcA mutant had a Fossariinae moderate competitive survival advantage in the reticuloendothelial system compared to the WT in all systemic organs examined following a p.o. or i.p. mixed infection (Figure 5B). In the majority of the mice, the arcA mutant was isolated in higher numbers than the WT, although these increases were not statistically significant (p > 0.05). The data generated with the competitive assays is in agreement with i.p. infection data, where the mice succumbed with similar kinetics after infection with arcA or WT bacteria. Figure 5 Virulence comparison of the WT and the arcA mutant in 6-8 week old C57BL/6 mice. (A) Single infection assays, where two groups of five mice per strain (WT and arcA mutant) were challenged

intraperitoneally using 250 CFU/mouse, as described in Materials and Methods. Percent survival is the number of mice surviving relative to the number of mice challenged at zero time; (B) Competitive infection assays, where groups of three 6-week-old mice were infected orally (p. o.) or i. p. with a 1:1 mixture of S. Typhimurium 14028 s and its isogenic arcA mutant. After 4 or 6 days following i.p. or p.o. infection, respectively, mice were euthanized and mesenteric lymph nodes (MLN), liver, and spleen were collected for enumeration of the WT and the mutant. The competitive index (CI) was calculated as described in the Materials and Methods. Discussion Although there are several reports on the regulation of specific genes by ArcA in non-virulent CYT387 price strains of E.