Supplementary MaterialsAdditional document 1: Table S1. and plasmids. Recently, we exhibited that incompatibility group (Inc) FIB plasmid-encoded iron acquisition systems (Sit and aerobactin) likely play an important role in persistence of in human intestinal epithelial cells (Caco-2). In this study, we sought to determine global transcriptome analyses of in iron-rich (IR) and iron-depleted (ID) growth conditions. Results The number of differentially-expressed genes were substantially higher for recipient (SE819) (transposases located on the IncFIB plasmid, ferritin and several regulatory genes were downregulated in TC in ID conditions. Enterobactin transporter (transposases and ArtA toxin of WT were downregulated in ID conditions. SDS-PAGE coupled with LC-MS/MS analyses revealed that siderophore receptor proteins such as chromosomally-encoded IroN and, IncFIB-encoded IutA were upregulated in WT and TC in ID growth conditions. Both chromosome and IncFIB plasmid-encoded SitA was overexpressed in WT, but not in TC or recipient in ID conditions. Increased expression of flagellin was detected in recipient and TC, but not in WT in ID conditions. Conclusion Iron concentrations in growth media influenced differential gene expressions both at transcriptional and translational levels, FTY720 (Fingolimod) including genes encoded around the IncFIB plasmid. Limited iron availability within the host may promote pathogenic to differentially express subsets of genes encoded by chromosome and/or plasmids, facilitating establishment of effective infections. Electronic supplementary FTY720 (Fingolimod) materials The web version of the content (10.1186/s12864-019-5768-0) contains supplementary materials, which is open to certified FTY720 (Fingolimod) users. is among the main foodborne pathogens in america [1, 2], frequently connected with multistate outbreaks associated with polluted foods and foods or pet pets such as for example turtle [3] and hedgehogs [4]. could cause an array of individual attacks, from mild gastroenteritis to invasive illnesses [5]. More than 2600 serovars have already been identified, largely FTY720 (Fingolimod) differing in host ranges and their ability to cause human infections [5]. serovars such as Enteritidis, Typhimurium, Newport, and Heidelberg can colonize intestines of a broad range of hosts including food generating animals and humans [6]. On the other hand, some serovars are host-restricted such as Typhi, Paratyphi, Gallinarum, Choleraesuis, Abortusovis and Dublin, which can only cause infections in one or few hosts [7]. Nonetheless, genetic factors that contribute to boarder host range and increased ability to cause invasive form of disease to Rabbit Polyclonal to MT-ND5 different serovars are still largely unknown. possess arrays of genes that aid in invasion, replication, and persistence inside the host cells [8]. Type III secretion systems (T3SS) are among the major factors that play functions in invasion and persistence in the host cells [9C11]. pathogenicity islands (SPIs) encode virulence factors, including T3SS, that are required during infections of host cells [12]. Genomes of acquire SPIs through different evolutionary processes via horizontal gene transfer (HGT). To date, 21 SPIs have been recognized in operon located on multiple virulence plasmids [20] likely contribute to increased virulence of during contamination FTY720 (Fingolimod) of host cells. However, the precise role of these virulence-associated plasmid factors of in contamination process remains to be decided. serovars encounter different challenging environments during host-pathogen interactions, including iron-limited conditions inside the host cells. Iron is not only an essential growth factor for many pathogenic bacteria [21], but also serves as a signaling element that regulates numerous genes, including virulence associated genes [22]. The grasp regulator, Fur (ferric uptake regulator), senses iron availability and controls gene expression as necessary, in response to physiological conditions [23C25]. Previous studies have shown that a Fur mutant attenuated the virulence and pathogenesis observed in vivo models for several pathogens [24, 26C29]. For most bacteria, iron acquisition is one of the key factors that determine their ability to survive in a host [30]. Bacteria that do not possess iron acquisition capability, may be removed by the host defense mechanisms [30]. Some of the common host defense.