I obtained in 2004 a PhD in Pharmacology from the University of Toulouse. My research interest in the laboratory of Digestive Biology (INSERM U531) was to decipher the signaling pathways involved in the initiation of colon and pancreas cancers.

In 2005, I joined the laboratory of Jeffrey Settleman at the Massachusetts General Hospital (MGH) Cancer Center, Harvard Medical School, in Boston (USA) where I characterized the differential drug response of mutated EGFR in non-small cell lung cancer. In 2006, I moved to the Surgery Department of the University of Melbourne (Australia) where I identified the crucial role of gastrin precursors in the tumor-initiating capacity of CD133-positive colon cancer cells.  In 2009, I have been recruited as a junior assistant professor (INSERM CRCN) to establish a research program aiming to identify therapeutic targets in colorectal cancer.

Since 2018, I lead a research group at the IRSD (Institut de Recherche en Santé Digestive) studying the interactions between the intestinal epithelium and the environment, either luminal or stromal. By combining morphological, functional, pharmacological and microfluidic approaches to 3D cell primocultures of colorectal organoids and fibroblasts, we study the interactions between the intestinal epithelium and the fibroblasts in the context of inflammatory bowel diseases and the risk of tumorigenesis.

Pro-resolution M2-like macrophages are critical for wound healing. Aging-associated systemic chronic inflammation alters their functions and favors the development of chronic wounds, a major morbidity in elderly patients. Basophils, rare circulating granulocytes known for their pro-inflammatory roles in allergic and parasitic diseases, can potently promote M2-like macrophage’s pro-resolution functions due to their high innate production of type 2 cytokines.

In this work in progress, we explore the roles of basophils in skin wound healing using mice models of specific basophil depletion or gene deletion, and reanalysis of published transcriptomic datasets. We show that basophils infiltrate skin wounds early during inflammation and express Interleukin 4 (IL-4) for at least three weeks. They inhibit the accumulation of pro-inflammatory monocytes/macrophages during the resolution phase in an IL-4 dependent manner and accelerate wound closure while favoring keratinocyte differentiation during re-epithelialization.In aged mice, basophils have a more activated and immature phenotype but unexpectedly show enhanced pro-resolution properties.

Thus, basophils display pro-resolution properties favoring the skin wound healing response in both adult and elder mice. Unraveling the molecular mechanisms controlling these properties may hold promise to restore optimal healing and resolution in the elderly.