Indole inhibits quorum sensing‐dependent phenotypes and virulence of acute hepatopancreatic necrosis disease‐causing Vibrio parahaemolyticus

Acute hepatopancreatic necrosis syndrome (AHPND) caused by a unique Vibrio parahaemolyticus strain (VPAHPND) has emerged as a serious disease of cultured shrimps and is causing great economic losses worldwide. In this work, the effects of indole on quorum sensing-dependent (QS) phenotypes of VPAHPND were assessed. In QS-inhibitory bioassay using biomonitor strains, indole could interfere with N-acyl homoserine lactones (AHL)-mediated violacein pigment production of Chromobacterium violaceum, and autoinducer-1 (AI-1) and autoinducer-2 (AI-2)-mediated QS response (bioluminescence) in V. campbellii. Further testing of indole with VPAHPND demonstrated significant decrease in the swimming and swarming motilities. In addition, VPAHPND grown in the presence of indole exhibited a reduction in biofilm formation, extracellular polymeric substances (EPSs) production and autoaggregation index. However, indole did not affect the ability of VPAHPND to use ferrous sulphate (FeSO4) as an iron source. Interestingly, indole reduced the expression of pirA (~2 fold), pirB (~2 fold), cpsA (~1.5 fold) and scrA (~1.7 fold) resulting in the reduction of toxin and capsule production. Lastly, indole-treated VPAHPND exhibited lower virulence towards an infected model and its specific host, Galleria mellonella larvae and Litopenaeus vannamei respectively. These demonstrated the effects of indole in reducing multiple QS-dependent phenotypes and virulence of VPAHPND. Thus, using indole, indole-containing compounds, or indole-producing organisms might be an attractive anti-virulence strategy to control infections caused by VPAHPND.