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Journal of Bacteriology, June 2008, p. 3940-3947, Vol. 190, No. 11
0021-9193/08/$08.00+0     doi:10.1128/JB.00086-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Norepinephrine Mediates Acquisition of Transferrin-Iron in Bordetella bronchiseptica{triangledown}

Mark T. Anderson{dagger} and Sandra K. Armstrong*

Department of Microbiology, University of Minnesota Medical School, Minneapolis, Minnesota 55455-0312

Received 17 January 2008/ Accepted 26 March 2008

Previous research demonstrated that the sympathoadrenal catecholamine norepinephrine could promote the growth of Bordetella bronchiseptica in iron-restricted medium containing serum. In this study, norepinephrine was demonstrated to stimulate growth of this organism in the presence of partially iron-saturated transferrin but not lactoferrin. Although norepinephrine is known to induce transcription of the Bordetella bfeA enterobactin catechol xenosiderophore receptor gene, neither a bfeA mutant nor a bfeR regulator mutant was defective in growth responsiveness to norepinephrine. However, growth of a tonB mutant strain was not enhanced by norepinephrine, indicating that the response to this catecholamine was the result of high-affinity outer membrane transport. The B. bronchiseptica genome encodes a total of 19 known and predicted iron transport receptor genes, none of which, when mutated individually, were found to confer a defect in norepinephrine-mediated growth stimulation in the presence of transferrin. Labeling experiments demonstrated a TonB-dependent increase in cell-associated iron levels when bacteria grown in the presence of 55Fe-transferrin were exposed to norepinephrine. In addition, TonB was required for maximum levels of cell-associated norepinephrine. Together, these results demonstrate that norepinephrine facilitates B. bronchiseptica iron acquisition from the iron carrier protein transferrin and this process may represent a mechanism by which some bacterial pathogens obtain this essential nutrient in the host environment.

* Corresponding author. Mailing address: Department of Microbiology, University of Minnesota, MMC 196, 420 Delaware Street S.E., Minneapolis, MN 55455-0312. Phone: (612) 625-6947. Fax: (612) 626-0623. E-mail: armst018{at}umn.edu

{triangledown} Published ahead of print on 4 April 2008.

{dagger} Present address: Department of Microbiology-Immunology, Northwestern University, Searle 3-420, S213, 303 E. Chicago Ave., Chicago, IL 60611.

Journal of Bacteriology, June 2008, p. 3940-3947, Vol. 190, No. 11
0021-9193/08/$08.00+0     doi:10.1128/JB.00086-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.





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