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Temperature and salinity modulate virulence and PirA gene expression of Vibrio parahaemolyticus , the causative agent of AHPND
Aquaculture International ( IF 2.9 ) Pub Date : 2021-02-26 , DOI: 10.1007/s10499-021-00654-0
Gabriela López-Cervantes , Píndaro Álvarez-Ruiz , Silvia Luna-Suárez , Antonio Luna-González , Héctor M. Esparza-Leal , Claudia Castro-Martínez , Carina Gámez-Jiménez , Jorge Soto-Alcalá

Global cultured shrimp production has sustained considerable losses due to acute hepatopancreatic necrosis disease (AHPND) caused by some strains of Vibrio that secrete PirAB binary toxin. Previous experiments have revealed changes in mortality due to AHPND under variable environmental conditions. In order to determine whether and how environmental factors affect the pathogenicity of a strain of Vibrio parahaemolyticus that causes AHPND (VpAHPND), a VpAHPND strain was grown at different temperatures (28, 30, and 33 °C) and proportions of NaCl (2.0, 3.0, and 3.5%). PirA gene expression was assessed in these bacterial cultures, and bioassays by immersion challenge were performed at 20, 30, and 35 practical salinity units (PSU). The results showed that salinities and temperatures tested do not inhibit VpAHPND growth. However, maximum PirA gene expression at 3.5, 3.0, and 2.0% NaCl reached 21.1, 13.0, and 0.03 millions of copies per ng of RNA, respectively, and at 28, 30, and 33 °C reached 48.5, 21.1, and 11.3 millions of copies per ng of RNA, respectively. Furthermore, the mortality rate in the bioassay challenges corresponded proportionally to the expression of the PirA gene, reaching 83.3, 46.6, and 0 mortality at 35, 30, and 20 PSU, respectively; and 90.0, 63.3, and 43.3 mortality at 28, 30, and 33 °C, respectively. These results indicate that NaCl concentration and temperature modify the expression of the PirA gene and regulate VpAHPND virulence. Since the virulence of VpAHPND is sensitive to environmental factors, it may be a potent target for therapeutic intervention in seasonal bacterial disease.



中文翻译:

温度和盐度调节副溶血性弧菌(AHPND的致病因子)的毒力和PirA基因表达

由于某些分泌PirAB二元毒素的弧菌菌株引起的急性肝胰腺坏死病(AHPND),全球养殖虾产量已遭受相当大的损失。先前的实验已经揭示了在变化的环境条件下,由于AHPND导致的死亡率变化。为了确定是否和因素如何影响环境的菌株的致病性副溶血性弧菌引起AHPND(VP AHPND),一个VP AHPND菌株在不同的温度(28、30和33°C)和一定比例的氯化钠(2.0、3.0和3.5%)下生长。在这些细菌培养物中评估了PirA基因的表达,并通过浸没攻击在20、30和35个实际盐度单位(PSU)上进行了生物测定。结果表明,所测试的盐度和温度不会抑制Vp AHPND生长。但是,PirA基因在3.5、3.0和2.0%NaCl的最大表达分别达到每ng RNA 21.1、13.0和0.03百万个拷贝,在28、30和33°C时分别达到48.5、21.1和11.3百万每ng RNA分别复制1个副本。此外,生物测定挑战中的死亡率与PirA基因的表达成正比,分别在35、30和20 PSU时分别达到83.3、46.6和0。分别在28、30和33°C下的死亡率分别为90.0、63.3和43.3。这些结果表明NaCl浓度和温度改变了PirA基因的表达并调节Vp AHPND毒力。由于Vp AHPND的毒力 对环境因素敏感,它可能是季节性细菌性疾病的有效治疗靶标。

更新日期:2021-02-26
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