The QseE-QseF two-component system: A key mediator of epinephrine-regulated virulence in the marine pathogen Edwardsiella piscicida.

Edwardsiella piscicida is a widespread pathogen that infects various fish species and causes massive hemorrhagic septicemia, resulting in significant property damage to the global aquaculture industry. Type III and VI secretion systems (T3/T6SS), controlled by the master regulator EsrB, are important virulence factors of E. piscicida that enable bacterial colonization and evasion from host immune clearance. In this study, we demonstrate that the QseE-QseF two-component system negatively regulated esrB expression by reanalysis of Tn-seq data. Moreover, the response regulator QseF directly bound to esrB promoter and inhibited the expression of T3/T6SS genes, especially in the presence of epinephrine. Furthermore, in response to the prompt increasing of epinephrine level, the host immune genes were delayed repressed and QseE-QseF timely inhibited the expression of T3/T6SS genes to evade immune clearance. In summary, this study enhances our understanding and knowledge of the conditional pathogenesis mechanism and virulence regulation network of E. piscicida.

PepA binds to and negatively regulates esrB to control virulence in the fish pathogen Edwardsiella piscicida.

As an important marine fish pathogen, Edwardsiella piscicida infects a broad range of fish species and causes substantial economic losses. The EsrA-EsrB two-component system is essential for the expression of type III and type VI secretion systems (T3/T6SSs), the key virulence determinants in the bacterium. In this study, a pull-down assay with the esrB promoter as bait was performed to identify the upstream regulators of esrB. As a result, PepA, a leucyl aminopeptidase, was identified as a repressor of EsrB and T3/T6SS expression. PepA bound to the esrB promoter region and negatively regulated the production of T3/T6SS proteins in early stages. Moreover, PepA was found to affect the in vivo colonization of E. piscicida in turbot livers through the regulation of EsrB expression. Collectively, our results enhance the understanding of the virulence regulatory network and in vivo colonization mechanism of E. piscicida. One sentence summary: PepA regulates EsrB expression in Edwardsiella piscicida.