2-fold) at the exponential growth phase

(Table 4). Adhesins can serve as potent biological effectors of inflammation, apoptosis and cell recognition, potentially contributing to the virulence and intracellular survival of Brucella spp. [44–46]. For instance, AidA adhesins are important for Bordetella pertussis recognition of host cells and in discriminating between macrophages and ciliated epithelial cells in humans [45]. Transporters. A large number of genes encoding find more transporters PS-341 in vivo (90 total) were altered in ΔvjbR or in response to the addition of C12-HSL to wildtype cultures (Table 3 and Additional File 3, Table S3). For example, an exporter of O-antigen (BMEII0838) was identified to be down-regulated 2.0-fold by the deletion of vjbR at an exponential growth phase, and 4.3 and 1.7-fold by the addition of C12-HSL to wildtype cells at exponential and stationary growth phases, respectively (Table 3). Among the 3-MA differently expressed transporters, ABC-type transporters were most highly represented, accounting for 62 out of the 90 transporter genes (including 15 amino acid transporters, 10 carbohydrate transporters and 16 transporters associated with virulence and/or defense mechanisms) (Table 3 and Additional File 3, Table S3). The correlation between ABC transporters and the ability to adapt to different environments is in tune with the ability of Brucella spp.

to survive in both extracellular and intracellular environments [47]. Transcription. Based on microarray analysis results, vjbR Amino acid deletion or the addition of C12-HSL to wildtype

cells altered the expression of 42 transcriptional regulators, comprised of 12 families and 14 two-component response regulators or signal transducing mechanisms (Table 2 and Additional File 3, Table S3). Among the transcriptional families altered by ΔvjbR and/or the addition of C12-HSL, 9 families (LysR, TetR, IclR, AraC, DeoR, GntR, ArsR, MarR and Crp) have been implicated in the regulation of virulence genes in a number of other pathogenic organisms [35, 48–55]. The regulation of virB has been reported to be influenced not only by the deletion of vjbR and C12-HSL treatment, but by several additional factors including integration host factor (IHF), BlxR, a stringent response mediator Rsh, HutC, and AraC (BMEII1098) [14, 15, 56–58]. The same AraC transcriptional regulator was found to altered by vjbR deletion and C12-HSL treatment of wildtype cells: down-regulated 1.8 and 2.8-fold at exponential phase (respectively), and up-regulated 1.9 and 1.5-fold (respectively) at the stationary growth phase (Table 2). Additionally, HutC (BMEII0370) was also found to be down-regulated at the exponential growth phase by the ΔvjbR mutant (1.8-fold), suggesting several levels of regulation for the virB operon by the putative QS components in B. melitensis (Additional File 3, Table S3).