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Acute hepatopancreatic necrosis disease (AHPND) caused by  Vibrio parahaemolyticus  resulted in great economic losses in global shrimp aquaculture. There is an urgent need for development of novel strategies to combat AHPND-causing  V. parahaemolyticus  ( Vp   AHPND ), given that one of the greatest challenges currently is the widespread use of antibiotics and subsequent emergence of multidrug-resistant bacteria. Here, we proposed a broad-spectrum antivirulence approach targeting a conserved histidine kinase, QseC, which has been demonstrated to activate virulence expression in several Gram-negative pathogens. Our results showed that QseC mediated the catecholamine stimulated effects on growth and flagellar motility of  Vp   AHPND . Transcriptome analysis revealed that QseC was involved in the global regulation of the virulence of  Vp   AHPND  as the Δ qseC  mutant exhibited a decreased expression of genes related to type IV pilin, flagellar motility, and biofilm formation, while an overexpression of type VI secretion system and cell wall biosynthesis. Subsequently, the bacterial catecholamine receptor antagonist LED209 not only neutralized the stimulatory effects of host catecholamines on the growth and motility of  Vp   AHPND   in vitro , but also attenuated the virulence of  Vp   AHPND  towards brine shrimp larvae and white shrimp  in vivo . Additionally, LED209 presented no interference with pathogen growth, nor the toxicity to the experimental animals. These results suggest that QseC can be an attractive antivirulence therapy target, and LED209 is a promising candidate for development of broad-spectrum antivirulence agents. This is the first study that demonstrated the role of QseC in the global regulation of  Vp   AHPND  infection and demonstrated the antivirulence potential of LED209, which provides insight into the use of an antivirulence approach for targeting not only  Vp   AHPND , but also a much larger collection of pathogenic bacteria.

frontiers in cellular and infection microbiology

QseC Inhibition as a Novel Antivirulence Strategy for the Prevention of Acute Hepatopancreatic Necrosis Disease (AHPND)-Causing Vibrio parahaemolyticus