Yersinia pestis transition metal divalent cation transporters

Abstract

An important component of host innate immunity is the ability to withhold iron (Fe) from invading pathogens. More recently, it has become clear that similar battles between the host and pathogen for manganese (Mn) and zinc (Zn) are also critical for the ability of bacterial pathogens to proliferate in hosts. As with Fe, an increasing number of bacterial pathogens have been shown to lose virulence when Zn or Mn transporters are mutated. Similar to many other bacterial pathogens, Yersinia pestis, the causative agent of bubonic, septicemic, and pneumonic plague, has multiple high-affinity transport systems for acquiring Fe 3+, Fe 2+, Mn, and probably Zn from the host. Proper homeostasis of divalent cation transition metals (Fe 2+, Mn, and Zn) may be critical for the progression of disease. Y. pestis likely achieves this homeostasis by (1) cation specificities of transporters; (2) using a combination of transporters; and (3) controlling expression of these transporters. This chapter will present new information on and review current knowledge of Fe 2+, Mn, and Zn uptake systems in Y. pestis, their regulation, and role in pathogenesis. © 2012 Springer Science+Business Media New York.