Work Group Christiane Wolz

Staphylococcus aureus: regulation, evolution and host interactions

The human pathogen Staphylococcus aureus asymptomatically colonizes the anterior nares of humans, but also causes a wide spectrum of diseases ranging from skin infections to major life-threatening acute infections. Additionally, S. aureus can cause chronic infections that require successful adaptation of the pathogen to the human host. We are interested in the regulatory mechanisms that influence the virulence, adaptation and in vivo survival of S. aureus.

Our publications at Pubmed.

Christiane Wolz at Google Scholar.

Ongoing research projects

Survival of S. aureus under stress and in macrophages

Several mechanisms allow S. aureus to survive under different stress conditions (e.g. nutrient limitation, antibiotics, within phagocytes). We use molecular approaches to understand how the pathogen copes with the challenging conditions encountered during infection or therapy. Regulatory circuits provided by quorum sensing, the stringent response or the alternative Sigma factor B are shown to be essential for stress adaptation and/or antibiotic tolerance. Survival strategies are analyzed on the single cell level since often only a subpopulation of bacteria is tolerant to the applied stresses. The two-component system SaeRS has been shown to be essential for macrophage escape through activation of the toxin encoding lukAB operon. We are analyzing the fate of bacteria and host cells after phagocytosis to elucidate the LukAB dependent mechanism leading to bacterial escape, host cell death and inflammation.

Members: Naisa Vetter, Calla Jickeli, Nathalya Korn
Funding: DFG, SPP2225

Role of phages for host adaption and evolution

For S. aureus, phages are the primary vehicles for horizontal gene transfer. They have a profound influence on virulence and resistance development, and therefore pathogen evolution. More than 90% of the human nasal isolates of S. aureus were found to carry Sa3int phages, which integrate as prophages into the bacterial hlb gene disrupting the expression of an important virulence factor. The virulence factor-encoding genes carried by the Sa3-phages are all highly human-specific and probably essential for bacterial survival in the human host. Very little is known about the basic mechanisms leading to mobilization and integration of these phages within different bacterial host strains. We investigate the complex mechanism involved in regulation and function of Sa3int phages, and especially the bacterial-phage interference. The elucidation of such mechanisms and the identification of potential phage regulators should help to understand the evolution and host adaptation of certain S. aureus lineages.

Members: Ronja Dobritz, Nathalya Korn
Funding: DFG, SPP2330