Plasma Catechofamines in Patients with Serious Postoperative Infection

Groves, A C; Griffiths, John C.; Leung, F Y; Meek, Robert N.

doi:10.1097/00000658-197307000-00020

Cited by 96 publications

(50 citation statements)

References 19 publications

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“…Levels of host stress hormones increase in response to infection (23,32), and an epinephrine/norepinephrine-mediated increase in sensitivity to LL-37 may act as a host defense system to combat infection, suggesting that bacterial sensing of stress hormones may be a double-edged sword; although bacteria can sense and exploit these molecules, the host can use the same signals to manipulate the bacteria. The effects of epinephrine and norepinephrine are likely to be complex, involving multiple effects on both bacteria and host to influence the outcome of infection.…”

Section: Discussionmentioning

confidence: 99%

“…Stress triggers an increase in plasma epinephrine levels (31), and plasma levels of epinephrine and norepinephrine have been reported to increase with patients suffering from postoperative sepsis compared to patients with no complications (32). Administration of norepinephrine and epinephrine to otherwise healthy subjects increases the severity of bacterial infections, including Clostridium perfringens in humans and enterohemorrhagic Escherichia coli (EHEC) in calves (42,63,65).…”

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confidence: 99%

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Genome-Wide Transposon Mutagenesis Identifies a Role for Host Neuroendocrine Stress Hormones in Regulating the Expression of Virulence Genes inSalmonella

et al. 2010

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Bacterial sensing of environmental signals plays a key role in regulating virulence and mediating bacteriumhost interactions. The sensing of the neuroendocrine stress hormones epinephrine (adrenaline) and norepinephrine (noradrenaline) plays an important role in modulating bacterial virulence. We used MudJ transposon mutagenesis to globally screen for genes regulated by neuroendocrine stress hormones in Salmonella enterica serovar Typhimurium. We identified eight hormone-regulated genes, including yhaK, iroC, nrdF, accC, yedP, STM3081, and the virulence-related genes virK and mig14. The mammalian ␣-adrenergic receptor antagonist phentolamine reversed the hormone-mediated effects on yhaK, virK, and mig14 but did not affect the other genes. The ␤-adrenergic receptor antagonist propranolol had no activity in these assays. The virK and mig14 genes are involved in antimicrobial peptide resistance, and phenotypic screens revealed that exposure to neuroendocrine hormones increased the sensitivity of S. Typhimurium to the antimicrobial peptide LL-37. A virK mutant and a virK mig14 double mutant also displayed increased sensitivity to LL-37. In contrast to enterohemorrhagic Escherichia coli (EHEC), we have found no role for the two-component systems QseBC and QseEF in the adrenergic regulation of any of the identified genes. Furthermore, hormone-regulated gene expression could not be blocked by the QseC inhibitor LED209, suggesting that sensing of hormones is mediated through alternative signaling pathways in S. Typhimurium. This study has identified a role for host-derived neuroendocrine stress hormones in downregulating S. Typhimurium virulence gene expression to the benefit of the host, thus providing further insights into the field of host-pathogen communication.

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Genome-Wide Transposon Mutagenesis Identifies a Role for Host Neuroendocrine Stress Hormones in Regulating the Expression of Virulence Genes inSalmonella

et al. 2010

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“…Septic patients frequently exhibit increased plasma concentrations of epinephrine and norepinephrine (NE), but show a decrease in the positive correlation that exists between catecholamine concentrations and systolic blood pressure (1). This disordered relationship between catecholamines and vascular tone is reflected by the diminished peripheral systemic vascular resistance that frequently occurs in sepsis (2,3).…”

Section: Introductionmentioning

confidence: 99%

Prolonged exposure of rat aorta to low levels of endotoxin in vitro results in impaired contractility. Association with vascular cytokine release.

McKenna¹

1990

J. Clin. Invest.

105

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Treatment of volunteers or animals with endotoxin in vivo results in reduced vascular reactivity to catecholamines. Endotoxin also causes liberation of the vasoactive cytokines interleukin-1 (IL-1) and tumor necrosis factor (TNF) from vascular smooth muscle and endothelial cells in culture. This study tested whether defects in contractility could be induced in isolated vascular tissue by prolonged exposure to endotoxin (1-100 ng/ml) in vitro, and whether IL-1 and TNF release by blood vessels is altered during the establishment of endotoxininduced contractile dysfunction. A concentration of endotoxin as low as 1 ng/mI suppressed contractions to norepinephrine (NE) and KCl; aortic sensitivity to NE also decreased. The presence of serum constituents or an intact endothelium were not necessary for endotoxin-induced vascular suppression. Aortas incubated with endotoxin liberated IL-1 and TNF in a dose-dependent fashion. The addition of dexamethasone or indomethacin during the incubations generally suppressed release of the cytokines and improved tissue reactivity to NE. The endotoxin-induced diminished vascular contraction and augmented IL-1 and TNF liberation required de novo protein synthesis; tissue incubated with endotoxin plus actinomycin D was completely shielded from the influence of endotoxin on vascular reactivity to NE. The association between endotoxininduced vascular cytokine release and diminished contraction suggests a possible role for cytokines derived from the vasculature in the regulation of contractile function. (J. Clin. Invest.

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“…Nanomolar concentrations of epinephrine and norepinephrine are found in the plasma of mammals, and in tissues the concentration of norepinephrine is dependent on the degree of sympathetic innervation at that site (78). Tissue injury is known to result in the release of norepinephrine from neurons (77), and high levels of circulating catecholamines and their metabolites have been correlated with severe bacterial infection (32) and onset of acute respiratory illness (33).…”

Section: Discussionmentioning

confidence: 99%

TheBordetellaBfe System: Growth and Transcriptional Response to Siderophores, Catechols, and Neuroendocrine Catecholamines

Anderson

Armstrong

2006

J Bacteriol

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Ferric enterobactin utilization by Bordetella bronchiseptica and Bordetella pertussis requires the BfeA outer membrane receptor. Under iron-depleted growth conditions, transcription of bfeA is activated by the BfeR regulator by a mechanism requiring the siderophore enterobactin. In this study, enterobactin-inducible bfeA transcription was shown to be TonB independent. To determine whether other siderophores or nonsiderophore catechols could be utilized by the Bfe system, various compounds were tested for the abilities to promote the growth of iron-starved B. bronchiseptica and induce bfeA transcription. The BfeA receptor transported ferric salmochelin, corynebactin, and the synthetic siderophores TRENCAM and MECAM. Salmochelin and MECAM induced bfeA transcription in iron-starved Bordetella cells, but induction by corynebactin and TRENCAM was minimal. The neuroendocrine catecholamines epinephrine, norepinephrine, and dopamine exhibited a remarkable capacity to induce transcription of bfeA. Norepinephrine treatment of B. bronchiseptica resulted in BfeR-dependent bfeA transcription, elevated BfeA receptor production, and growth stimulation. Pyrocatechol, carbidopa, and isoproterenol were similarly strong inducers of bfeA transcription, whereas tyramine and 3,4-dihydroxymandelic acid demonstrated low inducing activity. The results indicate that the inducer structure requires a catechol group for function and that the ability to induce bfeA transcription does not necessarily correlate with the ability to stimulate bacterial growth. The expanded range of catechol siderophores transported by the BfeA receptor demonstrates the potential versatility of the Bordetella Bfe iron retrieval system. The finding that catecholamine neurotransmitters activate bfeA transcription and promote growth suggests that Bordetella cells can perceive and may benefit from neuroendocrine catecholamines on the respiratory epithelium.

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Plasma Catechofamines in Patients with Serious Postoperative Infection

Cited by 96 publications

References 19 publications

Genome-Wide Transposon Mutagenesis Identifies a Role for Host Neuroendocrine Stress Hormones in Regulating the Expression of Virulence Genes inSalmonella

Genome-Wide Transposon Mutagenesis Identifies a Role for Host Neuroendocrine Stress Hormones in Regulating the Expression of Virulence Genes inSalmonella

Prolonged exposure of rat aorta to low levels of endotoxin in vitro results in impaired contractility. Association with vascular cytokine release.

TheBordetellaBfe System: Growth and Transcriptional Response to Siderophores, Catechols, and Neuroendocrine Catecholamines

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