Zu den Inhalten springen

AG Prof. Häcker

Prof. Dr. med. Georg Häcker

Telefon Labor +49 761 203-5363
Telefon Sekretariat +49 761 203-6532
Fax +49 761 203-6651
E-Mail georg.haecker@uniklinik-freiburg.de


1983 Allgemeine Hochschulreife
1990 Medizinisches Staatsexamen
1991 Promotion zum Dr. med., Universität Ulm
1992Approbation als Arzt
1993-1995 Stipendiat der Deutschen Forschungsgemeinschaft am Walter und Eliza Hall Institute for Medical Research, Melbourne, Australien
1995Research Officer am Walter and Eliza Hall Institute
1996-1998Wissenschaftlicher Angestellter / Assistenzarzt, Inst. f. Med. Mikrobiologie der TUM
1998 Habilitation und Venia legendi für Medizinische Mikrobiologie und Immunologie, Fakultät für Medizin der TUM
1998-2000Privatdozent, Oberarzt am Inst. f. Med. Mikrobiologie der TUM
2000-2009C3-Professor / Extraordinarius, Oberarzt am Inst. f. Med. Mikrobiologie der TUM
2002Facharzt für Mikrobiologie und Infektionsepidemiologie, Bayerische Landesärztekammer
07/2009 Ärztlicher Direktor der Abteilung Mikrobiologie und Hygiene, Universitätsklinikum Freiburg
Name Position Telefon E-Mail
Prof. Georg Häcker AG-Leiter 203- 6531 georg.haecker@uniklinik-freiburg.de
Dr. rer. nat. Arnim Weber Wiss. Angestellter 203- 5362 arnim.weber@uniklinik-freiburg.de
Dr. Aladin Haimovici Wiss. Angestellter 203- 6522 aladin.haimovici@uniklinik-freiburg.de
Dr. Collins Waguia Kontchou Wiss. Angestellter 203- 5358 collins.kontchou@uniklinik-freiburg.de
Dr. Abdul Moeed Wiss. Angestellter 203-6522 abdul.moeed@uniklinik-freiburg.de
Arlena Metz BTA 203- 5358 arlena.metz@uniklinik-freiburg.de
Julia Gregg Pharmazeut. Doktorandin 203- 5358 julia.gregg@uniklinik-freiburg.de
Tarek Amer Pharmazeut. Doktorand 203-5358 tarek.amer@uniklinik-freiburg.de
Benedikt Dörflinger Med. Doktorand 203- 5358 benedikt.doerflinger@uniklinik-freiburg.de
Christoph Höfer Med. Doktorand 203- 5358 christoph.hoefer@uniklinik-freiburg.de


PubMed Suchergebnis



Human infection means that the body comes into contact with a pathogen. In most cases this contact is first with a cell that is not part of the professional immune system, such as an epithelial cell of a mucosal surface or a keratinocyte of the skin. These cells can recognize the pathogen and signal alert: the complex process of inflammation is initiated, and professional immune cells are recruited, especially neutrophil granulocytes. The activation of myeloid cells (granulocytes, macrophages, dendritic cells) is then required for the activation of the adaptive immune system, where lymphocytes (B cells, T cells) react and help clear the pathogen.

We are mostly working on trying to understand bacterial infection. Bacteria may all be small and look similar, but they are actually incredibly diverse. Even bacteria that live on humans can be as different as plants and animals. A bacterium causing purulent infection (such as Staphylococcus aureus) is very (very) different from the bacterium causing tuberculosis (Mycobacterium tuberculosis), and so on. Accordingly, while some general principles apply, the human body’s response to different bacteria can be very different, and many aspects of how bacteria infect and how human cells respond and fight the infection are still unclear.

Within this general theme, we work on the following areas (more detail is given under the links):


Apoptosis is a form of cell death that occurs because the cell activates a specific signaling pathway, which kills it (it is in a way suicide). Apoptosis is a reaction to many stimuli, and apoptosis plays a role in infection. Some pathogens live inside human cells, and if the cell kills itself this may stop replication of the pathogen. Some bacteria have even evolved specific mechanisms that can prevent the infected cell killing itself. We find this interesting and are studying this interplay. In order to be able to study it we also analyze some of the basic questions of apoptosis, for instance how the release of apoptosis-inducing proteins from mitochondria is initiated. link

Sub-lethal apoptosis signalling

In many cases of infection there is actually little apoptosis induced. There is however an intriguing process initiated that we call sub-lethal apoptosis signalling: the same signalling pathway operates that also causes apoptosis but it is activated only a little. The cell therefore does not die but the same pathway, surprisingly, activates rather than kills the infected cell. When the apoptosis-apparatus signals at a sub-lethal level, infected epithelial cells produce cytokines (signalling proteins of the immune cells that can activate professional immune cells) and can even to a degree inhibit the growth of intracellular bacteria. Many aspects of this signalling process are at this stage not understood. link

Infections with Chlamydia

Chlamydia is an unusual bacterium: it can grow only inside a human cell. It grows inside a vacuole in the cytosol, has to avoid the cell’s defence systems and has to acquire nutrients and building blocks for its growth from the host cell. Chlamydia, most important Chlamydia trachomatis, is a frequent pathogen and causes severe eye infections (especially in Africa) as well as pelvic inflammation and infertility in women (worldwide). The life style of Chlamydia in the cell seems complicated but is very successful. We are trying to understand some of the mechanisms of how the bacteria interact with human epithelial cells in vitro. We are also using a mouse model to understand better what is happening during human infection with Chlamydia. link

Infections with Helicobacter

Helicobacter pylori is frequently found in the human stomach, and can (relatively rarely) cause ulcers and cancer. Many pathways are known through which Helicobacter interacts with human cells. We are looking at some new aspects of this interactions, hoping to understand more about how Helicobacter causes inflammation and also cancer. link

Myeloid cells

We are interested in the contribution that myeloid cells, especially neutrophils but also macrophages, make to the control of infections and to inflammation and tissue damage. We have, together with Susanne Kirschnek, set up a cell system where we can very nicely differentiate these cells from immortalised progenitor cells. This line of research is now mainly continued by the Kirschnek group. link