Sandra K. Armstrong, Ph.D.

Associate Professor

Department of Microbiology

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

armst018@umn.edu

612-625-6947 office
612-624-5177 lab

 

Research Interests:

Iron Acquisition in Pathogenic Bacteria

Virtually 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. Research in my laboratory is centered on Gram-negative bacterial pathogens of humans and nonhuman hosts.

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 nonhuman mammals, causing kennel cough in dogs, atrophic rhinitis in swine and snuffles in rabbits. These Bordetella species obtain iron supplied by their native iron-chelating siderophore, alcaligin, as well as siderophores produced by other microbial species (termed xenosiderophores) and from host iron containing compounds including heme and hemoglobin. These iron retrieval systems are expressed when the bacteria are starved for iron and they are further activated by cognate transcriptional regulators that respond to the presence of the specific iron compound. Our studies are aimed at analyzing the cis- and trans-acting determinants involved in transcriptional regulation of these iron utilization genes with the long range objective of understanding the processes governing the expression of different Bordetella iron acquisition in the host.

Francisella tularensis is a facultative intracellular bacterial pathogen that is highly infectious and can cause severe disease, however very little is known about its biology and pathogenic mechanisms. Our studies are aimed at defining the mechanisms by which F. tularensis satisfies its nutritional and metabolic requirements in the host environment.

Cell-Cell Signaling
Another project in my laboratory is the study of bacterial intercellular communication by the excretion and perception of signaling molecules. Recent experiments have identified molecules produced by Bordetella pertussis and Bordetella bronchiseptica that possess potent intercellular signaling activity. My lab is focused on determining whether Bordetella cells communicate with one another in the host during the course of infection, and whether this communication is required for optimal growth and regulation of the expression of known virulence factors.

Selected Recent Publications:

  • Anderson, M.T., Armstrong, S.K. 2006. The Bordetella bfe system: growth and transcriptional response to siderophores, catechols, and neuroendocrine catecholamines. J Bacteriol. 188(16):5731-40.
  • Brickman, T.J., Vanderpool, C.K., Armstrong, S.K. 2006. Heme transport contributes to in vivo fitness of Bordetella pertussis during primary infection in mice. Infect Immun. 74(3):1741-4.
  • Brickman, T.J., Armstrong, S.K. 2005. Bordetella AlcS transporter functions in alcaligin siderophore export and is central to inducer sensing in positive regulation of alcaligin system gene expression. J Bacteriol. 2005 Jun;187(11):3650-61.
  • Anderson, M.T. and S.K. Armstrong. 2004. The BfeR regulator mediates enterobactin-inducible expression of Bordetella enterobactin utilization genes. J. Bacteriol. 186:7302-7311.
  • Brickman, T.J., C.K. Vanderpool and S.K. Armstrong. 2004. Bordetella, p. 311-328. In Crosa, Mey and Payne,(ed.), Iron Transport in Bacteria; American Society for Microbiology, Washington, D.C.
  • Vanderpool, C.K. and S.K. Armstrong. 2004. Integration of environmental signals controls expression of Bordetella heme utilization genes. J. Bacteriol. 186:938-948.
  • Vanderpool, C.K. and S.K. Armstrong. 2003. Heme-responsive transcriptional activation of Bordetella bhu genes. J. Bacteriol. 185:909-917.
  • Brickman, T.J. and S.K. Armstrong. 2002. Alcaligin siderophore production by Bordetella bronchiseptica strain RB50 is not repressed by the BvgAS virulence control system. J. Bacteriol. 184:7055-7057.
  • Brickman, T.J. and S.K. Armstrong. 2002. Bordetella interspecies allelic variation in AlcR inducer requirements: identification of a critical determinant of AlcR inducer responsiveness and construction of an alcRCon mutant allele . J. Bacteriol. 184:1530-1539.
  • Brickman, T.J., H.Y. Kang, and S.K. Armstrong. 2001. Transcriptional activation of Bordetella alcaligin siderophore genes requires the AlcR regulator with alcaligin as inducer. J. Bacteriol. 183:483-489.
  • Vanderpool, C.K. and S.K. Armstrong. 2001. The Bordetella bhu locus is required for heme iron utilization. J. Bacteriol. 183:4278-4287.

Last modified on: October 24, 2006