Research group of Professor Martin Aepfelbacher

Research group of Professor Martin Aepfelbacher

Prof. Dr. Martin Aepfelbacher is the director of the Institute for Medical Microbiology, Virology and Hygiene at the University Medical Centre Hamburg-Eppendorf, currently one of the most modern hospitals in Europe (opened in February 2009). Research in the Aepfelbacher lab focuses on the cellular microbiology of the bacterial pathogens Yersinia enterocolitica and Staphylococcus aureus, the effect of bacterial toxins on the human vascular endothelium and the cell biology of macrophages.

Martin has an extensive background in scientific research. He studied at the Technical University of Munich (TUM) and the Ludwig-Maximilians-University (LMU), before working as a scientific assistant at the Medizinische Klinik Innenstadt, LMU. Martin then did postdoctoral research in the Howard Hughes Medical Institute, Seattle, USA, funded by a research stipend from the Deutsche Forschungsgemeinschaft. He was a scientific assistant at the Institute for the prevention of cardiovascular diseases, and the Max von Pettenkofer Institute for Hygiene and Medical Microbiology, LMU, before becoming an associate professor at the Max von Pettenkofer Institute. Martin was appointed to his current position as full professor and director of the Institute for Medical Microbiology, Virology and Hygiene, in 2005.

The Aepfelbacher lab works on various aspects of cellular microbiology. Pathogens frequently exploit the elaborate system of cell regulation for their advantage, i.e. to impede the immune system, grow in an intracellular niche and spread to other tissues or individual organisms. As well as contributing to the understanding of the molecular principles of pathogenicity, the lab aims to produce valuable tools for basic cell research and eventually for clinical applications.

Martin and his colleagues are particularly interested in the following research areas:

  • The cellular effects and molecular mechanisms of the Yersinia type III secretion system outer proteins (Yops) that regulate the Rho family of GTP-binding proteins. Yersinia species, which cause various human illnesses, use a variety of mechanisms to subvert host-cell responses and propagate disease. The Rho family of GTPases is commonly targeted by bacterial pathogens since these proteins mediate many essential immune cell functions, such as phagocytosis, chemotaxis and cytokine production.
  • The pathogenicity of S. aureus and S. epidermidis which interact with vascular endothelial cells during bacteraemia/sepsis. Researchers are investigating the mechanisms of S. aureus uptake, its processing and its potential to survive within the endothelium. This work is fundamentally important considering the increasing resistance of S. aureus to antibiotics.
GFP-actin
GFP-actin (green) transfected human umbilical vein endothelial cells (HUVEC) were infected with S. aureus expressing full length fibronectin binding protein A (FnBPA). FnBPA crucially determines the interaction of S. aureus with endothelial cells in vivo and in vitro. The top left panel shows a phase contrast reference image of a bacterial doublet which is associated with an actin tail as shown in the fluorescence image (top-right panel; arrow). From the boxed area, z-stacks were imaged and assembled into a 3D-image using Volocity software (bottom panel). By using the 3D rendering features of Volocity, they were able to show that the bacterial doublet (arrow) is almost completely engulfed by GFP-actin, although its top still extends into the extracellular space (scale bar: 10 μm).

YopO is a serine/threonine kinase required for Yersinia virulence. GFP-YopO (green) transfected HUVEC were infected with E. coli cellsexpressing Yersinia adhesin A (YadA; blue color) and were stained for f-actin (red). The movie shows a GFP-transfected cell (green) which contacts an untransfected cell (red due to f-actin staining). Using Volocity software, researchers showed that YadA induces bacterial uptake and colocalization of YopO with F-actin at the site of bacterial entry (colocalization of green and red color at the tip of the blue bacterial rod, shown in the center).

Martin says “We use the PerkinElmer spinning disk microscope and Volocity software for imaging the dynamics of the cytoskeleton, the localization and activation of RhoGTPases and intracellular vesicle transport in live cells infected with pathogenic bacteria. The bacteria we are most interested in are enteropathogenic Yersinia. It is intriguing to record how signaling mechanisms that are first activated by Yersinia surface adhesins in host cells are later down-regulated by Yersinia effector proteins injected into the cells. We also work on pathogenic S. aureus and S. epidermidis which use a plethora of different surface adhesins to invade cells on one hand but also to avoid uptake by cells on the other hand. The cell types we are most interested in are primary human endothelial cells and macrophages. Another project we are involved with is to aid Volker Heussler’s group, from the Bernhard Nocht Institute for Tropical Medicine in Hamburg, in imaging the morphology and dynamics of Plasmodia. The best known plasmodium is P. falciparum which causes tropical Malaria in millions of patients worldwide”.

Recent publications from the Aepfelbacher lab:

Stanway R R, Witt T, Zobiak B, Aepfelbacher M, Heussler V T (2009). Biol Cell. [Epub ahead of print] PMID: 19143588 [PubMed - as supplied by publisher]

Roppenser B, Röder A, Hentschke M, Ruckdeschel K, and Aepfelbacher M (2009). J Cell Sci. 122: 696 – 705

Schröder A, Schröder B, Roppenser B, Linder S, Sinha B, Fässler R, Aepfelbacher M (2006). Mol Biol Cell. 17: 5198 - 210

To find out more about research in the Aepfelbacher lab, please visit: http://www.uke.de/institute/infektionsmedizin/index_13928.php