Philip Rosenstiel

Philip Rosenstiel is a German medical doctor and an academic. He is director of the Institute of Clinical Molecular Biology and a professor of clinical molecular biology at Kiel University.

Rosenstiel is most known for his work on the pathophysiology of chronic inflammatory diseases, primarily focusing on developing innovative biomarkers and new therapeutic approaches. His work has been published in academic journals including Nature, Nature Genetics, Cell Metabolism and Immunity.

Education Rosenstiel obtained a degree in medicine in 2001 from Kiel University. During this time, he also went for training to Tufts University in Boston as part of a scholarship from the BMEP and the Studienstiftung. and is spokesperson of the Precision Health in Schleswig-Holstein, a governance body to foster clinical translational research in Schleswig-Holstein. Since 2022, he has been serving as vice-dean for research at the Medical Faculty in Kiel.

Research Rosenstiel has employed methods from systems immunology and utilized genomic techniques such as single-cell analysis to create novel biomarkers and explore innovative therapeutic strategies. He contributed to the pilot phase of the 1000 Genomes Project, participated in the German International Cancer Genome Consortium (ICGC) on malignant lymphoma and led the large European Horizon 2020 Project on Systems Medicine in Chronic Inflammation (SYSCID). He has authored publications with a specific focus on the pathophysiology of chronic inflammatory diseases, including articles in peer-reviewed journals. A particular focus has been on the role of autophagy and ER stress as basic principles of epithelial differentiation and Paneth cell function. His showed a link between the defective removal of RNA nucleotides during proliferation of intestinal epithelial cells, mucosal inflammation and colorectal cancer formation. With Josef Penninger and others, he demonstrated that a lack of the ACE2 enzyme, responsible for controlling the renin-angiotensin system, disrupts the balance of the amino acid tryptophan in the intestinal epithelium. This in turn leads to impaired antimicrobial peptide production in the gut, leading to increased susceptibility to colitis and intestinal inflammation. He has contributed to early clinical therapy developments, e.g. IL-6 transsignalling inhibition in IBD (olamkicept phase II trial) or sterile-filtered fecal material transfer for C. difficile infection.

Molecular profiling and biomarkers of disease Rosenstiel's work has also focused on biomarker development in chronic inflammatory diseases and cancer. Here, he mostly employed multi-omics techniques, e.g. transcriptomics and methylomics and microbiome analysis to develop predictions for individual trajectories of disease and to stratify patients for different targeted therapies. During the COVID-19 pandemic, he was founding member of the DeCOI consortium and led analyses, which identified megakaryocyte expression signatures as a marker for fatal disease course.

Awards and honors 2001 – Recipient of the Graduate stipend of the Novartis Stiftung für therapeutische Forschung 2003 – Hensel-Research Prize, Kiel University 2017 – Schleswig-Holstein Excellence Chair

Selected articles Hampe, J., Franke, A., Rosenstiel, P., Till, A., Teuber, M., Huse, K.... & Schreiber, S. (2007). A genome-wide association scan of nonsynonymous SNPs identifies a susceptibility variant for Crohn disease in ATG16L1. Nature genetics, 39(2), 207–211. Hashimoto, T., Perlot, T., Rehman, A., Trichereau, J., Ishiguro, H., Paolino, M.... & Penninger, J. M. (2012). ACE2 links amino acid malnutrition to microbial ecology and intestinal inflammation. Nature, 487(7408), 477–481. Aden, K., Tran, F., Ito, G. O., Sheibani-Tezerji, R., Lipinski, S., Kuiper, J. W.... & Rosenstiel, P. (2018). ATG16L1 orchestrates interleukin-22 signaling in the intestinal epithelium via cGAS–STING. Journal of Experimental Medicine, 215(11), 2868–2886. Bernardes, J. P., Mishra, N., Tran, F., Bahmer, T., Best, L., Blase, J. I.... & Rosenstiel, P. (2020). Longitudinal multi-omics analyses identify responses of megakaryocytes, erythroid cells, and plasmablasts as hallmarks of severe COVID-19. Immunity, 53(6), 1296–1314. Fazio, A., Bordoni, D., Kuiper, J. W., Weber-Stiehl, S., Stengel, S. T., Arnold, P.... & Rosenstiel, P. (2022). DNA methyltransferase 3A controls intestinal epithelial barrier function and regeneration in the colon. Nature Communications, 13(1), 6266.