Nanoparticle metal oxides represent a new class of important materials that are increasingly being developed for use in research and health-related applications. Highly ionic metal oxides are interesting not only for their wide variety of physical and chemical properties but also for their antibacterial activity. Although the in vitro antibacterial activity and efficacy of regular zinc oxides have been investigated, little is known about the antibacterial activity of nanoparticles of ZnO. Preliminary growth analysis data suggest that nanoparticles of ZnO have significantly higher antibacterial effects on Staphylococcus aureus than do five other metal oxide nanoparticles. In addition, studies have clearly demonstrated that ZnO nanoparticles have a wide range of antibacterial effects on a number of other microorganisms. The antibacterial activity of ZnO may be dependent on the size and the presence of normal visible light. The data suggest that ZnO nanoparticles have a potential application as a bacteriostatic agent in visible light and may have future applications in the development of derivative agents to control the spread and infection of a variety of bacterial strains.

The expression of genes involved in the pathogenesis of Staphylococcus aureus is controlled by global regulatory loci, including two-component regulatory systems and transcriptional regulators (e.g., sar family genes). Most members of the SarA family have been partially characterized and shown to regulate a large numbers of target genes. Here, we describe the characterization of sarZ, a sarA paralog from S. aureus, and its regulatory relationship with other members of its family. Expression of sarZ was growth phase dependent with maximal expression in the early exponential phase of growth. Transcription of sarZ was reduced in an mgrA mutant and returned to a normal level in a complemented mgrA mutant strain, which suggests that mgrA acts as an activator of sarZ transcription. Purified MgrA protein bound to the sarZ promoter region, as determined by gel shift assays. Among the sarA family of genes analyzed, inactivation of sarZ increased sarS transcription, while it decreased agr transcription. The expression of potential target genes involved in virulence was evaluated in single and double mutants of sarZ with mgrA, sarX, and agr. Northern and zymogram analyses indicated that the sarZ gene product played a role in regulating several virulence genes, particularly those encoding exoproteins. Gel shift assays demonstrated nonspecific binding of purified SarZ protein to the promoter regions of the sarZ-regulated target genes. These results demonstrate the important role played by SarZ in controlling regulatory and virulence gene expression in S. aureus.

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