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MICaB Faculty

Armstrong
Sandra K. Armstrong

Professor

Department of Microbiology and Immunology

University of Missouri-Columbia, 1986, Ph.D.

E-mail:armst018@umn.edu


Research Interests:


Bordetella biology and pathogenesis

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Bordetella pertussis, Bordetella bronchiseptica and Bordetella parapertussis are mammalian respiratory pathogens that are highly genetically-related Gram-negative members of the family Alcaligenaceae. B. pertussis, the agent of whooping cough (pertussis), is an obligate human pathogen. B. parapertussis causes respiratory infections in humans and sheep, and B. bronchiseptica infects a wide range of nonhuman mammals. These bacteria adhere to the cilia of the host respiratory tract, obtain nutrients, replicate and elaborate virulence factors that enable them to persist and become transmitted to new hosts.

To determine how these organisms successfully live in the host, we must understand their biology. Nearly all organisms require nutritive iron and its assimilation is essential for invading pathogenic bacteria to establish infection in the iron-limiting environment of the host. Bordetella species obtain iron supplied by their native iron-chelating siderophore, alcaligin, as well as siderophores produced by other microbial species, and from host iron containing compounds including heme. These iron retrieval systems are expressed when the bacteria are starved for iron and expression is further activated by cognate transcriptional regulators that respond to the presence of the specific iron compound. Recent studies have determined that these bacteria can utilize host neuroendocrine hormones, such as norepinephrine, for iron retrieval. Our studies are aimed at understanding the processes governing the expression of different Bordetella iron acquisition systems in the host during the course of infection.

Selected Recent Publications:

  • Hanawa, T., H. Yonezawa, H. Kawakami, S. Kamiya and S.K. Armstrong. 2013.  Role of Bordetella pertussis RseA in the cell envelope stress response and adenylate cyclase toxin release.  Pathog. Dis. In press.
  • Brickman, T.J. and S.K. Armstrong.  2012. Iron and pH-responsive FtrABCD ferrous iron utilization system of Bordetella species.  Mol. Microbiol. 86:580-593.
  • Armstrong, S.K., T.J. Brickman and R.J. Suhadolc.  2012. Involvement of multiple distinct Bordetella receptor proteins in the utilization of iron liberated from transferrin by host catecholamine stress hormones.  Mol. Microbiol. 84:446-462.
  • Brickman, T.J., C. A. Cummings, S-Y. Liew , D. A. Relman and S.K. Armstrong. 2011. Transcriptional profiling of the iron starvation response in Bordetella pertussis provides new insights into siderophore utilization and virulence gene expression. J. Bacteriol. 193:4798-4812.
  • Brickman, T.J. and S.K. Armstrong. 2009. Temporal signaling and differential expression of Bordetella iron transport systems: the role of ferrimones and positive regulators. BioMetals. 22:33-41.
  • Brickman, T.J., Hanawa T., Anderson M.T., Suhadolc, R.J. and S.K. Armstrong. 2008. Differential expression of Bordetella pertussis iron transport system genes during infection. Mol. Microbiol. 70:3-14.
  • Anderson, M.T. and S.K. Armstrong. 2008. Norepinephrine mediates acquisition of transferrin-iron in Bordetella bronchiseptica. J. Bacteriol. 190:3940-3947.