Our group’s research is focused on mechanisms of the inflammatory response in pancreatic beta cells in the context of type 1 and type 2 diabetes mellitus (T1DM/T2DM).

Inflammation is involved in the regulation of physiological responses to a variety of insults and serves as a protective control mechanism. The non-resolved inflammatory response plays a crucial role in the pathogenesis of many chronic autoimmune and metabolic diseases. It is related to an excessive production of pro-inflammatory mediators that influence the fundamental intracellular processes and cell-cell interactions. This may lead to loss of function and, in the long run, to the destruction of the tissues or organs involved.

We search for a link between inflammation, small lipid mediators and the function and fate of beta cells. We aim to understand the molecular basis of the autoimmune-mediated inflammation in T1DM and the low grade inflammation in T2DM. To analyze the role of inflammation we use various biochemical, cell- and molecular biology techniques in model cell lines (rat, mouse, human) as well as animal models of diabetes.

Our aims are:

  • Mechanisms of beta cell dysfunction and death in T1DM and T2DM
  • Signal transduction and metabolic pathways leading to inflammation of beta cells
  • Identification and characterization of inflammation sources under typical T1DM and T2DM conditions
  • Inflammation-mediated changes in pathophysiology of beta cells
  • Search for novel anti-inflammatory approaches to protect beta cells