BACKGROUND AND AIMS: Helicobacter pylori is an important human pathogen, infecting around half the population of the world. It has developed a number of refinements to allow it to persist in the human stomach. Catecholamine hormones have been shown to enhance growth of other bacterial species and are found in the gastric niche. We aimed to study growth enhancement of H. pylori by the human catecholamine hormones epinephrine and norepinephrine. METHODS: Growth studies were carried out in complex and defined media containing the hormones epinephrine, norepinephrine, and normetanephrine, the main host metabolite of norepinephrine. Bacterial density was measured by viable count or optical density. Intracellular ATP was measured using a bioluminescence assay technique. RESULTS: Both epinephrine and norepinephrine enhanced H. pylori growth in a dose-dependent strain-independent fashion, with norepinephrine being more effective than epinephrine. We showed a rapid (4 hours) dose-dependent effect on metabolic activity, as measured by intracellular ATP levels. We used a chemically defined medium to study mechanisms: chelation of ferric iron blocked H. pylori growth, which could be overcome by addition of norepinephrine. Disruption of the catechol group of norepinephrine abrogated its H. pylori-growth-promoting activity. CONCLUSIONS: Norepinephrine stimulates growth of H. pylori under otherwise growth-restricted conditions, and this effect is related to the ability of norepinephrine to bind ferric iron. This supports the notion that norepinephrine may aid H. pylori persistence in the stomach.
BACKGROUND AND AIMS: Helicobacter pylori is an important human pathogen, infecting around half the population of the world. It has developed a number of refinements to allow it to persist in the human stomach. Catecholamine hormones have been shown to enhance growth of other bacterial species and are found in the gastric niche. We aimed to study growth enhancement of H. pylori by the humancatecholamine hormones epinephrine and norepinephrine. METHODS: Growth studies were carried out in complex and defined media containing the hormones epinephrine, norepinephrine, and normetanephrine, the main host metabolite of norepinephrine. Bacterial density was measured by viable count or optical density. Intracellular ATP was measured using a bioluminescence assay technique. RESULTS: Both epinephrine and norepinephrine enhanced H. pylori growth in a dose-dependent strain-independent fashion, with norepinephrine being more effective than epinephrine. We showed a rapid (4 hours) dose-dependent effect on metabolic activity, as measured by intracellular ATP levels. We used a chemically defined medium to study mechanisms: chelation of ferric iron blocked H. pylori growth, which could be overcome by addition of norepinephrine. Disruption of the catechol group of norepinephrine abrogated its H. pylori-growth-promoting activity. CONCLUSIONS:Norepinephrine stimulates growth of H. pylori under otherwise growth-restricted conditions, and this effect is related to the ability of norepinephrine to bind ferric iron. This supports the notion that norepinephrine may aid H. pylori persistence in the stomach.
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Authors: Neil C Doherty; Feifei Shen; Nigel M Halliday; David A Barrett; Kim R Hardie; Klaus Winzer; John C Atherton Journal: J Bacteriol Date: 2010-01-08 Impact factor: 3.490
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Authors: Akeem Bartley; Tao Yang; Rebeca Arocha; Wendi L Malphurs; Riley Larkin; Kacy L Magee; Thomas W Vickroy; Jasenka Zubcevic Journal: Front Physiol Date: 2018-11-13 Impact factor: 4.566