The influence of molecular mediators and cellular components of the innate and adaptive immune system is increasingly recognized to play a significant role in the context of pulmonary and cardiovascular pathomechanisms. The acute respiratory distress syndrome (ARDS) is associated with the immigration of neutrophil granulocytes (PMN) and monocytes, which is controlled by chemokine formation and release from type I and type II alveolar epithelial cells. The pathophysiological regulation of this mechanism, and the resulting recruitment of cells of the innate immune system (e.g. PMN) into the alveolus, is insufficiently understood at the molecular and functional level in the context of inflammation. While our "air-liquid interface" and intravital microscopy platforms allow the functional testing of a "licensing" of PMN immigration by molecular regulators, the identification of possible key molecules is performed by single cell RNA sequencing (scRNAseq). This sequence of preclinical experiments in vitro and in vivo allows for a targeted identification of putative key molecules and a prediction as to whether these may influence the course and severity of ARDS in patients. 

Further projects of the junior research group address  

• the influence of B-cell mediated autoimmunity on different forms of pulmonary hypertension in preclinical small animal models and patient cohorts; and 
• the identification and characterization of bioactive and biodegenerative components of extracellular vesicles in patients with chronic kidney disease.