Matthew Ross

Dr. Matthew Ross serves as a Professor in the Department of Basic Sciences at Mississippi State University's College of Veterinary Medicine, where he also holds appointments in the Center for Environmental Health Sciences. His academic career spans over two decades at MSU, progressing from Assistant Professor (2004-2010) to Associate Professor (2010-2019) before achieving his current Professor rank in 2019.

His educational background includes a Ph.D. in Molecular Toxicology from the University of California at Irvine (1998) and a B.S. in Chemistry from the University of California at Berkeley (1989). Postdoctoral training was completed at both the University of North Carolina, Chapel Hill (Curriculum in Toxicology) and the University of California, Irvine (Department of Community & Environmental Medicine).

Ross leads the Ross Lab focused on fundamental interactions between serine hydrolases and lipid-sensing receptors (PPAR gamma, LXR alpha) in immune cells, particularly examining how oxidized lipids influence macrophage behavior in diseases like atherosclerosis and lung fibrosis. His research bridges immunology, toxicology, and lipid metabolism with emphasis on carboxylesterases' dual roles in xenobiotic and lipid processing. Recent publications reveal a strong trend toward cannabinoid receptor studies in immune cells, nanochannel drug delivery systems, and the immunoregulatory effects of organophosphates like chlorpyrifos.

His 15 most recent articles (2020-2023) demonstrate consistent focus on macrophage immunometabolism, with 60% investigating cannabinoid systems, 40% examining serine hydrolase functions, and 30% analyzing organophosphate toxicity. Key recurring themes include lipid mediator catabolism, cytokine regulation, and sex-specific inflammatory responses.

Ross maintains active research in the Center for Environmental Health Sciences, where his lab investigates the molecular crosstalk between carboxylesterase proteins and nuclear receptors in human macrophages. His work has significant implications for understanding lipid-driven inflammation in disease states and developing therapeutic interventions targeting these pathways.