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  • Programme Area 4

Glucocorticoids and Bioenergetics

  • 3R-Research
  • Autoimmune diseases
  • Fracture healing
  • Glucocorticoides
  • Immunometabolism

How do immune cells adapt to oxygen and nutrient deficiencies in inflamed tissue?

Acute and chronic inflammation can lead to a pronounced lack of oxygen and nutrients in the area of inflammation. How does the immune system manage to remain active despite this?

In acute inflammatory processes such as in the initial phase of bone healing -the fracture hematoma -, but also in chronic inflammation, such as rheumatoid arthritis, cells sometimes need more nutrients and oxygen than the body provides. This can lead to a pronounced lack of these vital substances at the site of inflammation.

About us

In order to be able to continue to functioning, especially immune cells which accumulate in the area of inflammation or in a fracture hematoma have a number of adaptation mechanisms. In this way, they manage to compensate their bioenergetic balance, which is decisive for the survival, development and functional efficiency of all cellular systems.

Our research group is investigating such mechanisms, as they undoubtedly play a central role not only in acute and chronic inflammation, but also in tissue regeneration. Furthermore, these adaptation mechanisms also offer possible starting points for new therapeutic strategies, as well as explanatory approaches for the modes of action of already approved anti-inflammatory drugs such as glucocorticoids.

The adaptation mechanisms of immune cells to an altered microenvironment in inflammatory events differ from species to species. In particular, disease processes in inflammatory joint diseases in humans and regeneration processes in bone healing cannot yet be adequately modelled in animals, making it difficult to transfer the results of these experiments to humans.

Therefore, we are establishing in vitro models based on human cells in order to mimic acute and chronic inflammation such as found in the initial phase of fracture healing and in the inflamed joint. To this end, we are generating a variety of different in vitro 3D disease models that exclusively consist of the involved human cells in shape with a 3D architecture under the influence of an inflammatory microenvironment.

Prospectively, the established models will offer an alternative to the animal models used in basic and applied biomedical research in order to i) study pathophysiological and regenerative processes of musculoskeletal diseases, ii) identify new potential target molecules and iii) test new therapeutic strategies and finally iv) reduce or even replace animal experiments.

Team

Groupleader:
Apl. Prof. Dr. rer. nat. Frank Buttgereit

Scientists:
Dr. Timo Gaber
Dr. Alexandra Damerau
Dr. Moritz Pfeiffenberger

PhD and MD students
Dana Alkhoury
Manuela Jakstadt
Min Liu
Gabriele May
Matilda Nieswandt
Johannes Plank
Jiayi Tian

Main cooperation partners

AG Winkler, AG Löhning, AG Chang

BCRT, Julius-Wolff-Institut

medac GmbH, Synaptic Lab

Buckley Lab, Oxford; AG Seibel, Sidney

SANOFI-Aventis, Pfizer, Novartis, Amgen, AbbVie, BMS, Lilly, J&J etc.