Research

Overview

Chronic pain is a critical public health issue affecting more than 100 million people worldwide but we know relatively little about the factors that differentiate those who develop chronic pain from those that do not. Understanding the individual differences that contribute to chronic pain risk could shed light on novel therapeutic strategies designed to treat chronic pain as a pathological process (i.e. a disease) rather than as a symptom. My work primarily focuses on identifying the genetic variations and patterns of gene expression that contribute to chronic pain risk across a number of pain types. We use a variety of methodologies to address questions in the lab, including behavioral modeling in animals, analysis of whole tissue and single cell gene expression, RNASeq, SNP genotyping in human subjects, human subjects pain phenotyping and whole genome methods. A critical component of our research program is translation into human subjects, so we often utilize clinical research collaborations to validate and explore genes identified in our animal and molecular lab studies. We not only work from the “bench-to-bedside” but also “bedside-to-bench” where we begin with clinically relevant candidate genes and use lab-based methods for determining the mechanisms underlying these genetic effects. Work from our lab has demonstrated that its expression and administration can attenuate acute and chronic sensitivity associated with inflammation. While we study inflammatory pain and pain following injury, most recently, we have focused on painful conditions that are not the result of another disease diagnosis. In these disorders, chronic pain IS the disease. Current studies are focusing on irritable bowel syndrome, a chronic painful condition where pain is poorly managed but affecting ~20% of the population. We have identified a set of candidate genes expressed in the bowel that may contribute to the generation and persistence of bowel hypersensitivity. By focusing on these identified molecules and genes, we hope to develop methods that halt the progression of chronic pathological pain states and reduce our dependence on ineffective treatments like opioids that come with a host of negative side effects as well as risk for addiction, misuse, and abuse.

• Grossi, V, Hyams, J., S, Glidden, N., C, Knight, B., E, Young, E., E. 2019. Characterizing Clinical Features and Creating a Gene Expression Profile Associated With Pain Burden in Children With Inflammatory Bowel Disease.. Inflammatory bowel diseases
• Baumbauer, K., M, Ramesh, D, Perry, M, Carney, K., B, Julian, T, Glidden, N, Dorsey, S., G, Starkweather, A., R, Young, E., E. 2020. Contribution of COMT and BDNF Genotype and Expression to the Risk of Transition from Acute to Chronic Low Back Pain.. The Clinical journal of pain
• Young, E., E, Lariviere, W., R, Belfer, I. 2012. Genetic basis of pain variability: recent advances.. Journal of medical genetics, 49 (1), 1-9
• Knight, B., E, Kozlowski, N, Havelin, J, King, T, Crocker, S., J, Young, E., E, Baumbauer, K., M. 2019. TIMP-1 Attenuates the Development of Inflammatory Pain Through MMP-Dependent and Receptor-Mediated Cell Signaling Mechanisms.. Frontiers in molecular neuroscience, 12, 220
• Adelman, P., C, Baumbauer, K., M, Friedman, R, Shah, M, Wright, M, Young, E, Jankowski, M., P, Albers, K., M, Koerber, H., R. 2019. Single-cell q-PCR derived expression profiles of identified sensory neurons.. Molecular pain, 15, 1744806919884496
• Recla, J., M, Bubier, J., A, Gatti, D., M, Ryan, J., L, Long, K., H, Robledo, R., F, Glidden, N., C, Hou, G, Churchill, G., A, Maser, R., S, Zhang, Z., W, Young, E., E, Chesler, E., J, Bult, C., J. 2019. Genetic mapping in Diversity Outbred mice identifies a Trpa1 variant influencing late-phase formalin response.. Pain, 160 (8), 1740-1753