Zinc homeostasis mechanism and its role in bacterial virulence capacity

Abstract

Zinc ion (Zn2+) is an essential cofactor required by numerous metalloenzymes and is important for structural and regulatory systems in bacterial cells. Zn2+ is a trace element: bacterial cells require only very small quantities. High concentrations of Zn2+ are toxic to microorganisms. In the environment, bacteria may be subject to conditions where Zn2+ is either very limited or s at a toxic level. Due to the limitation of Zn2+ or the toxic effect of high levels of free Zn2+ ions, the bacteria need to carefully control the intracellular level of Zn2+. This paper aims to determine the mechanisms bacteria use to maintain the intracellular Zn2+ concentration and the adaptation mechanisms used by bacteria to grow in a Zn2+-limited environment. The role of Zn2+ in bacterial pathogenesis and virulence capacity will also be discussed. It is known that in bacteria, Zn2+ homeostasis is maintained by Zn2+-uptake/import and Zn2+-efflux/export systems. These two systems provide a balance between the requirement for the metal and its toxicity and therefore is essential for bacterial growth and survival. Metal ions, including Zn2+ have been demonstrated to be involved in various bacterial pathogeneses. Moreover, there is increasing evidence for the importance of Zn2+ in the virulence of various bacteria. Zn2+ is shown to be involved in biofilm formation, bacterial motility, antibiotic resistance, and survival against oxidative stress. Therefore, the ability of bacterial cells to maintain a homeostasis of Zn2+ is crucial for their growth, survival and virulence capacity.