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Utilization of iron-catecholamine complexes involving ferric reductase activity in Listeria monocytogenes
V Coulanges1, P Andre, O Ziegler
1Département des Sciences de l'Aliment, Université Louis Pasteur, U.F.R. des Sciences Pharmaceutiques, Illkirch, France.
Abstract:
Listeria monocytogenes is a ubiquitous potentially pathogenic organism requiring iron for growth and virulence. Although it does not produce siderophores, L. monocytogenes is able to obtain iron by using either exogenous siderophores produced by various microorganisms or natural catechol compounds widespread in the environment. In the presence of tropolone, an iron-chelating agent, growth of L. monocytogenes is completely inhibited. However, the growth inhibition can be relieved by the addition of dopamine or norepinephrine under their different isomeric forms, while the catecholamine derivatives 4-hydroxy-3-methoxyphenylglycol and normetanephrine did not relieve the inhibitory effect of tropolone. Preincubation of L. monocytogenes with chlorpromazine and yohimbine did not antagonize the growth-promoting effect of catecholamines in iron-complexed medium. In addition, norepinephrine stimulated the growth-promoting effect induced by human transferrin in iron-limited medium. Furthermore, dopamine and norepinephrine allowed 55Fe uptake by iron-deprived bacterial cells. The uptake of iron was energy dependent, as indicated by inhibition of 55Fe uptake at 0 degrees C as well as by preincubating the bacteria with KCN. Inhibition of 55Fe uptake by L. monocytogenes was also observed in the presence of Pt(II). Moreover, when assessed by a whole-cell ferric reductase assay, reductase activity of L. monocytogenes was inhibited by Pt(II). These data demonstrate that dopamine and norepinephrine can function as siderophore-like compounds in L. monocytogenes owing to their ortho-diphenol function and that catecholamine-mediated iron acquisition does not involve specific catecholamine receptors but acts through a cell-bound ferrireductase activity.
Insights
Listeria monocytogenes can acquire iron using dopamine and norepinephrine, which act like siderophores. This process involves a cell-bound reductase and does not rely on specific catecholamine receptors.
Area of Science:
- Microbiology
- Bacterial Physiology
- Iron Metabolism
Background:
- Listeria monocytogenes requires iron for growth and virulence.
- This pathogen lacks siderophore production but can utilize exogenous iron sources.
- Environmental catechol compounds and exogenous siderophores are key iron acquisition mechanisms.
Purpose of the Study:
- To investigate the role of catecholamines in iron acquisition by Listeria monocytogenes.
- To determine if dopamine and norepinephrine can serve as iron-scavenging compounds.
- To elucidate the mechanism of catecholamine-mediated iron uptake.
Main Methods:
- Growth inhibition assays using tropolone and relief by catecholamines.
- Iron uptake studies using 55Fe with varying conditions (temperature, KCN, Pt(II)).
- Whole-cell ferric reductase activity assays.
Main Results:
- Dopamine and norepinephrine relieved tropolone-induced growth inhibition.
- These catecholamines facilitated 55Fe uptake in iron-deprived cells, an energy-dependent process.
- Pt(II) inhibited 55Fe uptake and ferric reductase activity, suggesting a role for this enzyme.
Conclusions:
- Dopamine and norepinephrine function as siderophore-like compounds in L. monocytogenes due to their ortho-diphenol structure.
- Catecholamine-mediated iron acquisition involves a cell-bound ferrireductase, not specific receptors.
- This highlights an alternative iron acquisition pathway for L. monocytogenes.