Head: PD Dr. rer. nat. Markus Hoffmann
Inflammation is essential for regenerative processes, such as disposal of damaged tissue, wound repair or fracture healing. If inflammation fails to stop timely, however, it becomes a pathological process. The research of our group aims to use a highly translational approach combining in vitro mechanistic studies with in vivo approaches and disease-orientated research to find master switches that determine resolution or chronicity of inflammation. A special focus is laid on the role of neutrophils/neutrophil extracellular traps (NETs) and the inflammation-related changes in tissue-resident cells.
Therapeutic amplification of NET formation
Although neutrophils are usually considered as pro-inflammatory cells, evidence is increasing that they also exert anti-inflammatory and immunoregulatory function. For instance, reactive oxygen species (ROS)-dependent formation of aggregated neutrophil extracellular traps (aggNETs) is crucial for resolution of inflammation of experimental arthritis and lupus. The underlying mechanisms involve NET-inherent enzymes that interrupt local inflammatory processes. Our research aims to employ these resolving properties of NETs for the treatment of chronic inflammatory conditions. To this end, we establish and refine protocols for tailored therapeutic amplification of NET formation with chemicals ROS inducers.
Tissue specific aspects of immune-mediated inflammatory diseases
Clinical observations in inflammatory diseases show that inflammation typically recurs at specific predilection sites which have been previously affected. This inflammatory memory of tissue is mediated by tissue resident mesenchymal cells (e.g. fibroblasts). Current projects aim to elucidate the molecular mechanisms of inflammatory memory and to establish therapeutic intervention strategies that target inflammatory tissue priming and prevent flares of inflammation.