Gou Yin, Fang Qingjian, Gu Hanjie, Tian Aijun, Li Jun, Wang Yan, Hu Yonghua
National Key Laboratory for Tropical Crop Breeding, Zhanjiang Experimental Station, Chinese Academy of Tropical Agricultural Sciences, Sanya, 572024 China.
Key Laboratory of Biology and Genetic Resources of Tropical Crops, Institute of Tropical Bioscience and Biotechnology, Chinese Academy of Tropical Agricultural Sciences, Haikou, 571101 China.
Mar Life Sci Technol. 2024 Jul 10;6(4):665-678. doi: 10.1007/s42995-024-00238-w. eCollection 2024 Nov.
Indole signaling has been regarded as a promising target to control aquatic diseases. However, the relationship between exogenous indole and the virulence of is obscure. is a facultative intracellular pathogen, and has been a model strain in aquaculture. In this study, we investigated the effect of exogenous indole on stress resistance and virulence of in the presence of and absence of endogenous indole (WT and Δ, respectively). Our results showed that exogenous indole reduced the resistance of WT against strong acidic stress, but enhanced that of Δ. Also, we found that exogenous indole abated viability of at high temperature, repressed bacterial biofilm formation, impaired bacterial envelope integrity, and weakened bacterial proliferation in macrophages, irrespective of the presence or absence of endogenous indole. These virulence-related phenotypes caused by exogenous indole are reasonably explained by the observation that exogenous indole downregulated the expressions of CpxRA and its target YccA via being responded by CpxA. The effects of exogenous indole on strong acid resistance are partially achieved by changing the expression of GadD, the key functional enzyme of acid resistance system (AR2). We believe that this is the first report about the impact of exogenous indole on strong acid stress and membrane integrity of pathogenic bacteria. Also, we reveal the likely mechanism by which exogenous indole regulates the expressions of virulence-related genes. These findings provide a new understanding on pathogenesis of and contribute to the prevention and control strategies of edwardsiellosis.
The online version contains supplementary material available at 10.1007/s42995-024-00238-w.
吲哚信号传导被认为是控制水生疾病的一个有前景的靶点。然而，外源性吲哚与[病原体名称]毒力之间的关系尚不清楚。[病原体名称]是一种兼性胞内病原体，一直是水产养殖中的模式菌株。在本研究中，我们研究了在存在和不存在内源性吲哚（分别为野生型和Δ[相关基因缺失型]）的情况下，外源性吲哚对[病原体名称]抗逆性和毒力的影响。我们的结果表明，外源性吲哚降低了野生型对强酸性应激的抗性，但增强了Δ[相关基因缺失型]的抗性。此外，我们发现，无论是否存在内源性吲哚，外源性吲哚都会降低[病原体名称]在高温下的活力，抑制细菌生物膜形成，损害细菌包膜完整性，并削弱细菌在巨噬细胞中的增殖。外源性吲哚引起的这些与毒力相关的表型可以通过以下观察结果得到合理的解释：外源性吲哚通过被CpxA响应而下调CpxRA及其靶标YccA的表达。外源性吲哚对强酸抗性的影响部分是通过改变抗酸系统（AR2）的关键功能酶GadD的表达来实现的。我们认为这是关于外源性吲哚对病原菌强酸应激和膜完整性影响的首次报道。此外，我们揭示了外源性吲哚调节毒力相关基因表达的可能机制。这些发现为[病原体名称]的发病机制提供了新的认识，并有助于爱德华氏菌病的防控策略。
在线版本包含可在10.1007/s42995-024-00238-w获取的补充材料。
