No effect of N-acyl homoserine lactones disruption by lactonase enzyme on the virulence of Vibrio anguillarum towards sea bass (Dicentrarchus labrax) and brine shrimp (Artemia franciscana)

Abstract

Quorum sensing (QS) is a bacterial communication system in which bacteria coordinate the expression of certain genes in response to the presence of small signal molecules. Some signal molecules called autoinducers are found to regulate several phenotypes of bacteria. The molecules used for the QS system of Vibrio anguillarum are supposed to regulate their pathogenic genes. However, it is not well understood how exactly the virulence gene of V. anguillarum is regulated by the QS molecules to date. To address this question, one of the QS molecules of the NB10 strain of V. anguillarum called N-acyl homoserine lactones (AHLs) was disrupted by a lactonase enzyme to verify its role on their virulence. The effects of AHLs degradation in vitro were investigated by measuring its effect on growth and virulence factors production (lipase, phospholipase, and caseinase) and in vivo by verifying its effect on sea bass and Artemia larvae infection. Lactonase enzyme degraded AHLs of NB10; yet that degradation had no effect on the cell growth and production of the tested virulence factors. Similarly, challenge tests demonstrated that larval mortality was not significantly lower by lactonase treatment. Therefore, these observations indicated that virulence gene expression of V. anguillarum and its virulence are not regulated by the AHL-mediated QS system; either different molecules or other factors are associated with the virulence regulation of V. anguillarum towards the tested life stages of sea bass and Artemia.