The core focus of our research group is to uncover the cellular and molecular drivers of chronic and fibrosing interstitial lung diseases (ILDs), with a primary emphasis on idiopathic pulmonary fibrosis (IPF) and sarcoidosis. We investigate how epithelial dysfunction, immune–mesenchymal crosstalk and aberrant tissue repair mechanisms contribute to disease initiation and progression in pulmonary fibrosis. While in sarcoidosis we are interested in multinucleated giant cell formation and how dysfunction phagosome maturation and TH17.1 cell contribute.
In IPF, our work has identified key players in this process, including alveolar macrophages (via CCL18 secretion) and reprogrammed airway basal epithelial cells (Fig.1). We also established the roles of alveolar macrophage–fibroblast signaling loops, as major contributors of the fibrotic microenvironment.
By integrating bronchoalveolar lavage (BAL) transcriptomics, single-cell analysis, spatial transcriptomics, proteomics and longitudinal clinical data, we identify molecular signatures and biomarkers that enhance our ability to stratify patients, predict disease progression, optimize therapeuthic intervention and/or transplant timing.
To complement in vivo and in silico approaches, our group has pioneered the use of human precision-cut lung slices (PCLS) as a high-fidelity, ex vivo model of lung disease. A key innovation of our platform is the ability to maintain PCLS in culture for extended periods beyond 14 days and up to 42 days, enabling:
This advancement positions PCLS as a powerful tool for drug screening, biomarker validation, mechanistic studies and personalized medicine.
Importantly, our PCLS work aligns with the FDA’s strategic roadmap to reduce animal testing, supporting the regulatory shift toward New Approach Methodologies (NAMs) that offer greater human relevance in preclinical safety and efficacy studies.
Beyond IPF, our research extends to other chronic and inflammatory lung diseases, including:
Across all projects, our goal is to translate molecular insights into precision medicine strategies, grounded in human-relevant models and clinically meaningful outcomes.
Prasse’s work on BAL gene expression and epithelial reprogramming in IPF was featured at the Pulmonary Fibrosis Foundation Summit.
https://www.pulmonaryfibrosis.org/pff-summit
Social Media