Response of Vibrio cholerae to the Catecholamine Hormones Epinephrine and Norepinephrine

InEscherichia coli orSalmonella 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 thatVibrio 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 ofV. 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 O2 or superoxide. InE. coli , the QseC sensor kinase, which detects the autoinducer AI-3, also senses E or NE. The genome ofV. cholerae O395 comprises an open reading frame coding for a putative protein with 29% identity toE. coli QseC. Quantitative reverse transcriptase PCR (qRT-PCR) experiments revealed increased transcript levels of theqseC -like gene and ofpomB , a gene encoding a structural component of the flagellar motor complex, under the influence of E or NE. Phentolamine blocks the response ofE. coli QseC to E or NE. AV. cholerae mutant devoid of theqseC -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 thatV. cholerae senses the stress hormones E and NE. A sensor related to the histidine kinase QseC fromE. coli is identified and is proposed to participate in the sensing of NE.IMPORTANCE Vibrio 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. PathogenicV. 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 thatV. cholerae , like some enterobacteria, benefits from these stress hormones and possesses a sensor to recognize them.