The Salmonella enterica serovar Typhimurium QseB response regulator negatively regulates bacterial motility and swine colonization in the absence of the QseC sensor kinase

Bearson, Bradley L.; Bearson, Shawn M.D.; Lee, In Su; Brunelle, Brian W.

doi:10.1016/j.micpath.2010.03.005

Cited by 70 publications

(65 citation statements)

References 27 publications

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“…The products of these two genes are predicted to be homologs of the quorum-sensing TCST system QseBC of E. coli. In many bacteria, the QseBC TCST system serves as an important regulatory system involved in metabolism, virulence, biofilm development, and motility (6,7,15,36,47,49,65,80). Here we have renamed QseBC to FirRS in NTHI since we have found no role for this TCST system in quorum-sensing or biofilm development (data not shown) and NTHI is nonmotile.…”

Section: Resultsmentioning

confidence: 99%

“…The QseBC system responds to the host hormones epinephrine, norepinephrine, and/or bacterial autoinducer 3 (AI-3) in Salmonella enterica serovar Typhimurium, Aeromonas hydrophila, Edwardsiella tarda, and Aggregatibacter actinomycetemcomitans (7,47,65,80). QseBC also has a role in biofilm production in E. coli, A. hydrophila, and A. actinomycetemcomitans (47,65,75).…”

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confidence: 99%

“…QseBC also has a role in biofilm production in E. coli, A. hydrophila, and A. actinomycetemcomitans (47,65,75). QseB regulates motility (6,7,15,47,74,80) and also functions as an autoregulator, activating the expression of the qseBC operon in E. coli (14,49,56). Importantly, QseBC affects virulence in A. hydrophila, A. actinomycetemcomitans, E. tarda, and E. coli (47,49,65,80), and swine colonization by S. Typhimurium (6, 7).…”

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confidence: 99%

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Characterization of a Ferrous Iron-Responsive Two-Component System in Nontypeable Haemophilus influenzae

et al. 2012

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Nontypeable Haemophilus influenzae (NTHI), an opportunistic pathogen that is commonly found in the human upper respiratory tract, has only four identified two-component signal transduction systems. One of these, an ortholog to the QseBC (quorum-sensing Escherichia coli) system, was characterized. This system, designated firRS, was found to be transcribed in an operon with a gene encoding a small, predicted periplasmic protein with an unknown function, ygiW. The ygiW-firRS operon exhibited a unique feature with an attenuator present between ygiW and firR that caused the ygiW transcript level to be 6-fold higher than the ygiW-firRS transcript level. FirRS induced expression of ygiW and firR, demonstrating that FirR is an autoactivator. Unlike the QseBC system of E. coli, FirRS does not respond to epinephrine or norepinephrine. FirRS signal transduction was stimulated when NTHI cultures were exposed to ferrous iron or zinc but was unresponsive to ferric iron. Notably, the ferrous iron-responsive activation only occurred when a putative iron-binding site in FirS and the key phosphorylation aspartate in FirR were intact. FirRS was also activated when cultures were exposed to cold shock. Mutants in ygiW, firR, and firS were attenuated during pulmonary infection, but not otitis media. These data demonstrate that the H. influenzae strain 2019 FirRS is a two-component regulatory system that senses ferrous iron and autoregulates its own operon.

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confidence: 99%

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Characterization of a Ferrous Iron-Responsive Two-Component System in Nontypeable Haemophilus influenzae

et al. 2012

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“…The human pathogen enterohemorrhagic E. coli (EHEC) (12,29) and the human or animal pathogen S. enterica serovar Typhimurium (4,5,(34)(35)(36) possess the membrane-embedded QseC receptor, which senses the catecholamine hormones epinephrine (E) and norepinephrine (NE) or bacterial autoinducer 3 (AI-3). The binding of one of these compounds leads to an expression of virulence genes in bacteria (29).…”

Section: Discussionmentioning

confidence: 99%

“…The stress-associated mammalian hormones epinephrine (E) and norepinephrine (NE), for example, support the growth (1-3) and motility (4,5) of the enterobacteria Escherichia coli, Salmonella enterica serovar Typhimurium, and Klebsiella pneumoniae (6), of Pseudomonas aeruginosa (7,8), and of some Vibrio species (9) in a serum-based bacteriostatic medium. As E and NE share structural similarities to the bacterial catechol siderophores-a benzene ring with two adjacent hydroxyl groups-it was suggested that these stress hormones may be involved in the binding and uptake of iron by bacteria, thus promoting growth or motility (1)(2)(3)(4)(5). Recently, the mechanism by which catecholamine hormones bind to the ferric ion in complex with lactoferrin or transferrin was elucidated.…”

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Response of Vibrio cholerae to the Catecholamine Hormones Epinephrine and Norepinephrine

et al. 2015

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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 stressassociated 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. Stress enhances the susceptibility of a mammalian host to infection by bacteria. The stress-associated mammalian hormones epinephrine (E) and norepinephrine (NE), for example, support the growth (1-3) and motility (4, 5) of the enterobacteria Escherichia coli, Salmonella enterica serovar Typhimurium, and Klebsiella pneumoniae (6), of Pseudomonas aeruginosa (7,8), and of some Vibrio species (9) in a serum-based bacteriostatic medium. As E and NE share structural similarities to the bacterial catechol siderophores-a benzene ring with two adjacent hydroxyl groups-it was suggested that these stress hormones may be involved in the binding and uptake of iron by bacteria, thus promoting growth or motility (1-5). Recently, the mechanism by which catecholamine hormo...

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Neurotransmitters: The Critical Modulators Regulating Gut–Brain Axis

Mittal

Debs

Patel

et al. 2017

Journal Cellular Physiology

421

287

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Neurotransmitters including catecholamines and serotonin play a crucial role in maintaining homeostasis in the human body. Studies on these neurotransmitters mainly revolved around their role in the “fight or flight” response, transmitting signals across a chemical synapse and modulating blood flow throughout the body. However, recent research has demonstrated that neurotransmitters can play a significant role in the gastrointestinal (GI) physiology. Norepinephrine (NE), epinephrine (E), dopamine (DA), and serotonin have recently been a topic of interest because of their roles in the gut physiology and their potential roles in gastrointestinal and central nervous system pathophysiology. These neurotransmitters are able to regulate and control not only blood flow, but also affect gut motility, nutrient absorption, gastrointestinal innate immune system, and the microbiome. Furthermore, in pathological states such as inflammatory bowel disease (IBD) and Parkinson’s disease, the levels of these neurotransmitters are dysregulated, therefore causing a variety of gastrointestinal symptoms. Research in this field has shown that exogenous manipulation of catecholamine serum concentrations can help in decreasing symptomology and/or disease progression. In this review article, we discuss the current state-of-the-art research and literature regarding the role of neurotransmitters in regulation of normal gastrointestinal physiology, their impact on several disease processes, and novel work focused on the use of exogenous hormones and/or psychotropic medications to improve disease symptomology.

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The Salmonella enterica serovar Typhimurium QseB response regulator negatively regulates bacterial motility and swine colonization in the absence of the QseC sensor kinase

Cited by 70 publications

References 27 publications

Characterization of a Ferrous Iron-Responsive Two-Component System in Nontypeable Haemophilus influenzae

Characterization of a Ferrous Iron-Responsive Two-Component System in Nontypeable Haemophilus influenzae

Response of Vibrio cholerae to the Catecholamine Hormones Epinephrine and Norepinephrine

Neurotransmitters: The Critical Modulators Regulating Gut–Brain Axis

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