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Philippe Lesnik PhD Biomedical
Course and current status
Dr. Lesnik is Group Leader (DR2) within INSERM Unit 939 "Dyslipidemias, Inflammation and Atherosclerosis in Metabolic Disease" based within University of Pierre and Marie Curie at L’Hôpital de La Pitié in Paris. He obtained his Ph.D. in Molecular and Cellular Biology from University of Pierre and Marie Curie in 1993, then from 1994-1999 worked as a postdoctoral investigator in INSERM U321 under the direction of Dr. John Chapman. From 1999-2002 he was a Visiting Investigator at the Gladstone Institute of Cardiovascular Disease, University of California. In 2002 he returned to Dr Chapman’s INSERM Unit and now currently leads one of the major research team within the Unit. Major research interests of his team are lipid-inflammatory relationships in leucocytes, particularly with respect to dendritic cells, macrophages and foam cells, post-prandial lipid metabolism and human macrophage cholesterol homeostasis.
Scientific summary
Dr. Lesnik’s main research interest is the role of macrophages, dendritic cells and related leucocytes in the development of atherosclerosis. He places a particular emphasis on the role of cellular players of the innate and adaptive immunity, cellular regulatory networks influenced by environmental and metabolic changes and key cellular lipid sensors/receptors (Pattern recognition receptors and ABC transporters). Dr. Lesnik developed two transgenic mouse strains (CD11c-hBcl2 and CD68-hBcl2) to explore the relationships between the immune system, particularly macrophages and dendritic cells, and atherosclerosis. He has also successfully used mouse models to explore other aspects of leukocyte involvement in atherosclerosis, including studies of the role of fractalkine in the recruitment of monocytes to lesions, and of the impact of macrophage apoptosis on lesion growth at different stages of development. He also developed an atherosclerosis-susceptible, autoimmune mouse and demonstrated that the associated enhanced immune system activation and arterial inflammation accelerates atherosclerosis.
