Acute hepatopancreatic necrosis syndrome (AHPND) caused by a unique Vibrio parahaemolyticus strain (VP_AHPND) 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 VP_AHPND 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 VP_AHPND demonstrated significant decrease in the swimming and swarming motilities. In addition, VP_AHPND 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 VP_AHPND 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 VP_AHPND 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 VP_AHPND. Thus, using indole, indole-containing compounds, or indole-producing organisms might be an attractive anti-virulence strategy to control infections caused by VP_AHPND.

中文翻译：

---

吲哚抑制引起副溶血性弧菌的急性肝胰腺坏死疾病的群体感应依赖性表型和毒力

由独特的副溶血性弧菌（VP _AHPND ）引起的急性肝胰腺坏死综合征（AHPND ）已成为养殖虾的一种严重疾病，并在全球范围内造成巨大的经济损失。在这项工作中，评估了吲哚对 VP _AHPND的群体感应依赖 (QS) 表型的影响。在使用生物监测菌株的 QS 抑制性生物测定中，吲哚可干扰N-酰基高丝氨酸内酯 (AHL) 介导的紫色色杆菌 ( Chromobacterium v​​iolaceum) 的紫罗兰素色素产生，以及 autoinducer-1 (AI-1) 和 autoinducer-2 (AI-2) 介导的V中的 QS 响应（生物发光）。 坎贝利_ 用 VP _{AHPND进一步测试吲哚}表明游泳和蜂拥运动显着降低。此外，在吲哚存在下生长的 VP _AHPND表现出生物膜形成、细胞外聚合物 (EPS) 产生和自聚集指数的减少。然而，吲哚不影响VP _AHPND使用硫酸亚铁(FeSO ₄ ) 作为铁源的能力。有趣的是，吲哚降低了pirA（~2 倍）、pirB（~2 倍）、cpsA（~1.5 倍）和scrA（~1.7 倍）的表达，从而导致毒素和胶囊产生减少。最后，吲哚治疗的 VP _AHPND分别对受感染的模型及其特定宿主、大毒蛾幼虫和南美白对虾表现出较低的毒力。_{这些证明了吲哚在降低 VP AHPND}的多种 QS 依赖性表型和毒力方面的作用。因此，使用吲哚、含吲哚化合物或产生吲哚的生物体可能是控制由 VP _AHPND引起的感染的一种有吸引力的抗毒策略。