
معرفی
Lara Longobardi, PhD is an Associate Professor of Medicine within the Division of Rheumatology, Allergy, and Immunology at the University of North Carolina at Chapel Hill School of Medicine. Her research laboratory is situated in the Thurston Building on the UNC campus in Chapel Hill, North Carolina.
Dr. Longobardi received her undergraduate education at Federico II University, completed her PhD at the Second University of Naples in Italy, and held a Research Scholar position through the Oak Ridge Associated Universities (ORAU) Fellowship at Vanderbilt University.
Her primary research focuses on signal pathways involved in degenerative diseases like osteoarthritis (OA), as well as inflammatory and autoimmune conditions.
- She investigates the role of inflammatory chemokines and cytokines, particularly MCP5/MCP1 and their receptor CCR2, in joint tissue degeneration following trauma
- She utilizes a murine model of post-traumatic OA based on medial meniscus destabilization
- Her work examines how blocking chemokine signaling affects cartilage, bone, and pain measurement post-injury
- She collaborates with researchers from The Johnston County Osteoarthritis Project, TARC, and the Second University of Naples
Analysis of Dr. Longobardi's publication history reveals a strong focus on osteoarthritis mechanisms, cartilage biology, and regenerative medicine approaches. Her work spans fundamental molecular research on chemokine pathways, translational studies on biomarkers, and potential therapeutic interventions. Recent publications demonstrate expansion into immunology with her SARS-CoV-2 antibody research, while maintaining her core focus on joint degeneration and inflammation.
Dr. Longobardi's research program involves multiple collaborative projects including The Johnston County Osteoarthritis Project with Dr. Joanne Jordan, collaborations with Peng Liu and TARC, and work with Rosanna Filosa from the Second University of Naples, Italy. Her laboratory employs various murine models of arthritis including destabilization of medial meniscus, collagenase-induced arthritis, monosodium iodoacetate-induced arthritis, and collagen-induced arthritis.
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