Khalil Bdeir, PhD

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Research Associate Professor of Pathology and Laboratory Medicine
Department: Pathology and Laboratory Medicine

Contact information
505c Stellar Chance Bldg.
422 Curie Blvd
Department of Pathology and Laboratory Medicine
Perelman School of Medicine
University of Pennsylvania
Philadelphia, PA 19104/6082
Office: 215-898-2428
Fax: 215-573-0252
Education:
B.Sc.Pharm (Pharmacy)
Hebrew Univ. of Jerusalem, School of Pharmacy, Jerusalem, Israel, 1987.
M.Sc.Pham (Pharmacokinetics and Pharmacodynamics)
Hebrew Univ. of Jerusalem, School of Pharmacy, Jerusalem, Israel, 1990.
PhD (Biochemistry and Pharmacology)
Hebrew Univ. of Jerusalem, Hadassah Medical School, Jerusalem, Israel, 1996.
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Description of Research Expertise

The main focus of my research has been on the link between inflammation and thrombosis, with an emphasis on the pathobiology of alpha-defensins, plasminogen activator system and recently developmental endothelial locus-1 (Del-1) and its role in chronic and acute thrombo-inflammatory diseases like thrombotic stroke, acute chest syndrome (ACS) in sickle cell disease. I was among the first to characterize a transgenic mouse that expresses human alpha-defensins in its neutrophils. It has been our underlying hypothesis that the lack of alpha-defensins in mouse neutrophils, the most abundant protein secreted by their activated human counterparts, together with the rapid apoptosis that these cells undergo in tissue, has led to an under-appreciation of their role in inflammatory and thrombotic disorders. I have extensive experience in the production, purification and characterization of human alpha defensins and Del-1 and diverse in vivo animal models of thrombosis, pulmonary embolism, acute lung injury, and ischemic stroke. My recent focus is the role of Del-1 as a pulmonary endothelial cell derived negative regulator of inflammation in the pathogenesis of ACS. My collaborators provided me with Del-1 knock out and over-expressors mice, and I have generated a novel CRISPR mouse with a single amino acid mutation essential for integrin binding and function of Del-1.
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Last updated: 02/23/2024
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