The Kdp system is widely distributed among bacteria. In Escherichia coli, the Kdp-ATPase is a high-affinity K ؉ uptake system and its expression is activated by the KdpDE two-component system in response to K ؉ limitation or salt stress. However, information about the role of this system in many bacteria still remains obscure. Here we demonstrate that KdpFABC in Staphylococcus aureus is not a major K ؉ transporter and that the main function of KdpDE is not associated with K ؉ transport but that instead it regulates transcription for a series of virulence factors through sensing external K ؉ concentrations, indicating that this bacterium might modulate its infectious status through sensing specific external K ؉ stimuli in different environments. Our results further reveal that S. aureus KdpDE is upregulated by the Agr/RNAIII system, which suggests that KdpDE may be an important virulence regulator coordinating the external K ؉ sensing and Agr signaling during pathogenesis in this bacterium.

No abstract

BackgroundThe apicomplexan parasite Toxoplasma gondii can infect and replicate in virtually any nucleated cell in many species of warm-blooded animals; T. gondii has elaborate mechanisms to counteract host-cell apoptosis in order to maintain survival and breed in the host cells.MethodsUsing microarray profiling and a combination of conventional molecular approaches, we investigated the levels of microRNAs (miRNAs ) in human macrophage during T. gondii infection. We used molecular tools to examine Toxoplasma-upregualted miRNAs to revealed potential signal transducers and activators of transcription 3(STAT3) binding sites in the promoter elements of a subset of miRNA genes. We analysed the apoptosis of human macrophage with the functional inhibition of the STAT3-binding miRNAs by flow cytometry.ResultsOur results demonstrated differential alterations in the mature miRNA expression profile in human macrophage following T. gondii infection. Database analysis of Toxoplasma-upregulated miRNAs revealed potential STAT3 binding sites in the promoter elements of a subset of miRNA genes. We demonstrated that miR-30c-1, miR-125b-2, miR-23b-27b-24-1 and miR-17 ~ 92 cluster genes were transactivated through promoter binding of the STAT3 following T. gondii infection. Importantly, functional inhibition of selected STAT3-binding miRNAs in human macropahges increased apoptosis of host cells.ConclusionsA panel of miRNAs is regulated through promoter binding of the STAT3 in human macrophage and these miRNAs are involved in anti-apoptosis in response to T. gondii infection.

Staphylococcus aureus is an important human pathogen that causes a variety of diseases, ranging from localized skin infections to life-threatening systemic infections. The success of S. aureus as a pathogen is partly due to its ability to adhere to a wide range of host tissues by binding to host extracellular matrix proteins such as fibrinogen, fibronectin, and collagen. Staphylococcus aureus expresses two proteins that can bind specifically to fibrinogen, clumping factors A and B (ClfA and ClfB). Repressor of toxins (Rot) is known to be a global regulator of virulence gene expression in S. aureus. The translation of Rot is regulated by the staphylococcal accessory gene regulator (Agr) quorum-sensing system. In this study, we demonstrated that Rot and the Agr system in S. aureus NCTC8325 can affect the bacterial binding ability to human fibrinogen (Fg) under different bacterial growth phases. Our real-time RT-PCR results indicated that both Rot and the Agr system have no significant effect on clfA expression. However, Rot is an activator of clfB, and Agr/RNAIII can regulate clfB expression via Rot. Gel shift data further suggested that Rot might regulate clfB expression by directly binding to the promoter region of clfB. Moreover, Rot and the Agr system exhibited consistent regulatory effects on clfB transcription and bacterial Fg-binding ability, suggesting that Rot and the Agr system might affect bacterial Fg-binding ability mainly through regulating clfB transcription.