Neta Shlezinger, Zuckerman Faculty Scholar, publishes paper in of the National Academy of Sciences
The Hebrew University of Jerusalem
Subverting the host immune system is a major task for any given pathogen to assure its survival and proliferation. For the opportunistic human pathogen Bacillus cereus (Bc), immune evasion enables the establishment of potent infections. In various species of the Bc group, the pleiotropic regulator PlcR and its cognate cell–cell signaling peptide PapR7 regulate virulence gene expression in response to fluctuations in population density, i.e., a quorum-sensing (QS) system. We demonstrate that the QS peptidic inhibitor blocks host immune system–mediated eradication by reducing the expression of PlcR-regulated major toxins similarly to the profile that was observed for isogenic strains. Our findings provide evidence that Bc infectivity is regulated by QS circuit-mediated destruction of host immunity, thus reveal an interesting strategy to limit Bc virulence and enhance host defense.