Evolution has equipped organisms with sophisticated tools that can prevent or limit the impact of infectious disease and that directly target and destroy pathogenic microorganisms after infection. In our group we focus on two aspects of the host response to infection: innate immunity affording resistance and mechanisms that preserve parenchymal functionality and integrity affording Disease Tolerance to infection.
In the field of Innate Immunity, we study long term and prevailing adaptive responses to sequential inflammatory stress with a special emphasis on innate immune training. We have recently shown that also host-derived alarmins, such as the iron-containing molecule heme, impose long-lasting adaptation on the cellular and organismal level regulating the inflammatory reaction and disease severity to subsequent bacterial sepsis.
In the field of Disease Tolerance, we study mechanisms that maintain organ function in severe infections with a special emphasis on the molecular pathogenesis of the sepsis, that is the worse course of infectious disease. We specifically investigate adaptive and maladaptive host metabolic responses triggered during sepsis in order to understand mechanisms for new therapeutic strategies to ensure survival and organ integrity during sepsis and run the first ever clinical trial that target Disease Tolerance Mechanisms (EPOS-1; https://clinicaltrials.gov/ct2/show/NCT05033808).
We also perform direct clinical research and study severe systemic infections such as S.aureus bacteremia.
We apply state-of-the-art techniques in immunology, genome engineering (e.g. using CRISPR-Cas9) cell biology and molecular biology, in vivo and in vitro infection models, metabolic cages and are collaborating with other groups to perform systems biology approaches such as transcriptomics, targeted metabolomics and single cell analysis and single nuclei ATAC sequencing, ChIP sequencing.