Quorum Sensing and Self-Quorum Quenching in the Intracellular Pathogen<i>Brucellamelitensis</i>

Abstract

<div><p><i>Brucella</i> quorum sensing has been described as an important regulatory system controlling crucial virulence determinants such as the VirB type IV secretion system and the flagellar genes. However, the basis of quorum sensing, namely the production of autoinducers in <i>Brucella</i> has been questioned. Here, we report data obtained from the use of a genetic tool allowing the <i>in situ</i> detection of long-chain <i>N</i>-acyl-homoserine lactones (AHL) activity at single bacterium level in <i>Brucella melitensis</i>. These data are consistent with an intrinsic production of AHL by <i>B. melitensis</i> in low concentration both during <i>in vitro</i> growth and macrophage infection. Moreover, we identified a protein, named AibP, which is homologous to the AHL-acylases of various bacterial species. <i>In vitro</i> and during infection, expression of <i>aibP</i> coincided with a decrease in endogenous AHL activity within <i>B. melitensis</i>, suggesting that AibP could efficiently impair AHL accumulation. Furthermore, we showed that deletion of <i>aibP</i> in <i>B. melitensis</i> resulted in enhanced <i>virB</i> genes expression and VirB8 production as well as in a reduced flagellar genes expression and production of FlgE (hook protein) and FliC (flagellin) <i>in vitro</i>. Altogether, these results suggest that AHL-dependent quorum sensing and AHL-quorum quenching coexist in <i>Brucella</i>, at least to regulate its virulence.</p></div

    Similar works