Response of Vibrio cholerae to the Catecholamine Hormones Epinephrine and Norepinephrine
Response of Vibrio cholerae to the Catecholamine Hormones Epinephrine and Norepinephrine
复制标题
DOI：
10.1128/jb.00345-15
复制
发表时间：
2015-12-01
影响因子：
3.2
通讯作者：
Steuber, Julia
中科院分区：
文献类型：
--
作者：
Halang, Petra;Toulouse, Charlotte;Steuber, Julia
在大肠杆菌或沙门氏菌中，应激相关的哺乳动物激素肾上腺素（E）和去甲肾上腺素（NE）通过与QseC传感器蛋白相互作用触发信号级联反应。在这里，我们表明，霍乱弧菌，霍乱的病原体，表现出特定的E和NE的反应。这些儿茶酚酸盐（0.1mM）增强了霍乱弧菌菌株O395在含有小牛血清的培养基中的软琼脂上的生长和游泳运动性，所述培养基模拟宿主内的环境。在生长过程中，激素被转化为降解产物，包括肾上腺色素形成的自氧化与O-2或超氧化物。在大肠在大肠杆菌中，检测自身诱导物AI-3的QseC传感器激酶也感测E或NE。霍乱弧菌O395基因组含有一个开放阅读框，编码一个与大肠杆菌同源性为29%的蛋白质。coli QseC.定量逆转录酶PCR（qRT-PCR）实验显示，增加的转录水平的qseC样基因和pomB，基因编码的鞭毛电机复合体的结构组成部分，在E或NE的影响。酚妥拉明阻断E. coli QseC转化为E或NE。缺乏qseC样基因的霍乱弧菌突变体在E的存在下保留了酚妥拉明敏感的运动性，而NE刺激的运动性不再被酚妥拉明抑制。我们的研究表明，霍乱弧菌感觉应激激素E和NE。对大肠杆菌组氨酸激酶QseC相关的传感器进行了研究。大肠杆菌被确定，并提出参与感NE。重要霍乱弧菌是一种革兰氏阴性细菌，可能会导致霍乱，一种严重的疾病，由于腹泻和呕吐引起的急性脱水，死亡率高。致病性霍乱弧菌菌株具有毒力因子，如霍乱毒素（CTX）和响应于宿主提供的信号而产生的毒素共调节菌毛（TCP）。在致病性肠细菌中，人类宿主的应激相关激素肾上腺素（E）和去甲肾上腺素（NE）作为产生毒力因子的信号分子，并通过从宿主螯合铁来促进细菌生长。在这里，我们表明，霍乱弧菌，像一些肠杆菌，受益于这些应激激素，并拥有一个传感器来识别它们。
In Escherichia coli or Salmonella enterica, the stress-associated mammalian hormones epinephrine (E) and norepinephrine (NE) trigger a signaling cascade by interacting with the QseC sensor protein. Here we show that Vibrio cholerae, the causative agent of cholera, exhibits a specific response to E and NE. These catecholates (0.1 mM) enhanced the growth and swimming motility of V. cholerae strain O395 on soft agar in a medium containing calf serum, which simulated the environment within the host. During growth, the hormones were converted to degradation products, including adrenochrome formed by autooxidation with O-2 or superoxide. In E. coli, the QseC sensor kinase, which detects the autoinducer AI-3, also senses E or NE. The genome of V. cholerae O395 comprises an open reading frame coding for a putative protein with 29% identity to E. coli QseC. Quantitative reverse transcriptase PCR (qRT-PCR) experiments revealed increased transcript levels of the qseC-like gene and of pomB, a gene encoding a structural component of the flagellar motor complex, under the influence of E or NE. Phentolamine blocks the response of E. coli QseC to E or NE. A V. cholerae mutant devoid of the qseC-like gene retained the phentolamine-sensitive motility in the presence of E, whereas NE-stimulated motility was no longer inhibited by phentolamine. Our study demonstrates that V. cholerae senses the stress hormones E and NE. A sensor related to the histidine kinase QseC from E. coli is identified and is proposed to participate in the sensing of NE.IMPORTANCEVibrio cholerae is a Gram-negative bacterium that may cause cholera, a severe illness with high mortality due to acute dehydration caused by diarrhea and vomiting. Pathogenic V. cholerae strains possess virulence factors like the cholera toxin (CTX) and the toxin-coregulated pilus (TCP) produced in response to signals provided by the host. In pathogenic enterobacteria, the stress-associated hormones epinephrine (E) and norepinephrine (NE) of the human host act as signal molecules for the production of virulence factors and promote bacterial growth by the sequestration of iron from the host. Here we show that V. cholerae, like some enterobacteria, benefits from these stress hormones and possesses a sensor to recognize them.