Funding: DFG (HE 3546/6-1) (1/2018 bis 12/2022)

The importance of post-translational protein glycosylation in the pathogenesis of S. aureus infections is not well understood yet. In this project, we further analyze the importance of glycosylation of S. aureus surface proteins, such as Pls in biofilm formation and tissue colonization.

Funding: IZKF Münster Hei2/027/18 (01/2018 bis 12/2020)

Extracellular (e)DNA is a major structural component of staphylococcal biofilms. We identified a novel mechanism of eDNA generation in the coagulase-negative Staphylococcus lugdunensis mediated by the competence gene comEB. comEB is part of the comEABC competence operon. The S. lugdunensis comEB mutant has a severe defect in biofilm formation with strongly decreased eDNA levels as visualized by confocal laser scanning microscopy (see Figure A). The underlying mechanisms in the eDNA-dependent biofilm formation mediated by the competence operon comEABC were studied in more detail.

Funding: IZKF Münster Hei2/027/14 (01/2014 bis 10/2017) 

Most bacterial glycoproteins identified to date are virulence factors of pathogenic bacteria. The importance of protein glycosylation in the pathogenesis of S. aureus infections remains largely unknown. We identified the plasmin-sensitive protein Pls from S. aureus as a glycoprotein and found that the glycosyltransferases GtfC/GtfD and GtfE/GtfF are involved in its glycosylation. The role of Pls glycosylation in different aspects of S. aureus pathogenicity was studied in more detail. 

Funding: DFG (HE 3546/2-2) (06/2013 bis 03/2017)

In this prolongation project, we characterized the previously identified Atl-mediated staphylococcal internalization mechanism by human host cells in detail (see Figure B). 

Funding: DFG (HE 3546/3-1) (07/2007 bis 10/2011) 

In this project, we identified domains of the S. aureus extracellular fibrinogen-binding proteins coagulase and Efb binding to Candida biofilms. The coagulase leads to the conversion of fibrinogen to fibrin, which may shield the Candida cells against the host immune defense as suggested by CLSM (see Figure C). Indeed, phagocytosis assays demonstrated a reduced phagocytosis rate of Candida in the presence of coagulase or Efb. The inhibition of phagocytosis of Candida cells by coagulase and Efb via two distinct mechanisms suggests that S. aureus might be beneficial for Candida to persist as it helps Candida to circumvent the host immune system. 

Funding: IZKF Münster Hei2/022/09 (01/2009 bis 10/2012)

In this project, we identified and characterized the 238 kDa S. aureus surface protein C (SasC) that mediated the formation of huge cell aggregates indicative of intercellular adhesion, higher attachment to polystyrene, and enhanced biofilm formation.

Funding: DFG (HE 3546/2-1) (01/2006 bis 12/2008)

In this project, we described a novel mechanism of staphylococcal internalization that involves the major autolysin/adhesin Atl and AtlE from S. aureus and S. epidermidis, respectively, and we identified the human heat shock cognate protein Hsc70 as putative host cell receptor in Atl-mediated uptake of staphylococcal cells. 

Funding: DFG (GRK 1409: The International Graduate School: "Molecular interactions of pathogens with biotic and abiotic surfaces“) (10/2006 bis 09/2016)

In this long-term project, we studied different aspects of staphylococcal biofilm formation in detail.

Förderung: DFG-Projekt im SFB 293, Teilprojekt A6 (1/2006 bis 12/2008)

Funding: IZKF Münster Hei2/042/04 (01/2004 bis 10/2007) 

Förderung: DFG-Projekt im SFB 293, Teilprojekt A6 (1/2003 bis 12/2005)

Förderung: Medizinische Fakultät der Universität Münster: "Innovative Medizinische Forschung (IMF)" (2000-2001)