Marc Chanson is a Full Professor at the University of Geneva's Faculty of Medicine, Department of Cell Physiology and Metabolism. He leads a research group focused on cystic fibrosis and gap junctions, investigating the role of intercellular communication in inflammatory responses and host-pathogen interactions in the context of cystic fibrosis. Education: PhD from University of Geneva (1991) Post-doctoral training at Albert Einstein College of Medicine (New York, USA) Post-doctoral training at Medical College of Pennsylvania (Philadelphia, USA) Post-doctoral training at Utrecht University (Netherlands) Professor Chanson's research centers on the role of gap junctions and intercellular communication in cystic fibrosis pathophysiology, particularly focusing on host-pathogen interactions in airway epithelial cells. His work combines cell biology, electrophysiology, and imaging approaches using primary human respiratory epithelium cultures and genetically modified animal models. He has made significant contributions to understanding how transmembrane channels specialized in direct intercellular communication function in cystic fibrosis contexts. His recent publications (2020-2024) show a consistent focus on cystic fibrosis airway epithelium, particularly examining Pseudomonas aeruginosa infections, epithelial barrier function, and the role of connexins and pannexins in host-pathogen interactions. The research spans molecular mechanisms, therapeutic approaches including bacteriophage therapy, and fundamental understanding of cell communication pathways in disease contexts. Advising and Grants: Supervised multiple PhD students including Idris T. (2023), Bou Younes M-TA. (2022), Sofoluwe A. (2019) Collaborates with researchers across multiple institutions on cystic fibrosis and gap junction research Active in developing therapeutic approaches for cystic fibrosis complications Professor Chanson leads a research laboratory at the Centre Médical Universitaire (CMU) in Geneva, where his team investigates the links between CFTR mutations and pulmonary disorders, with particular focus on how gap junctions may represent pharmacological targets to modulate innate immune responses in cystic fibrosis.
