My primary interest lies in the understanding of gene x environment interactions on pain outcomes, with a particular focus on stress and injury/inflammation as environmental factors. Genetic factors have been shown to contribute significantly to variability in the response to painful stimuli. We are beginning to unravel the individual gene candidates and the families of genes that contribute to differences in pain responses. Using genetic correlation analysis with standard inbred strains of mice in addition to whole-genome quantitative trait locus (WTL) mapping with genetic reference populations as our most powerful tools, we are able to explore the genetic contribution to both somatic and visceral pain behaviors. Stress and inflammation can both modulate pain responses to various stimuli, and it is likely that different genes are involved in pain under normal conditions and the modulation of pain through environmental factors. Most recently, my research has focused on these issues as they relate to bowel pain after inflammation using animal models of Inflammatory Bowel Disease (IBD). The candidate genes identified in preclinical models can then be examined in clinical populations to determine whether these genes contribute to pain susceptibility in IBD patients. The goal is to further understand the mechanisms underlying persistent bowel pain and to use this knowledge to identify novel therapeutic targets to reduce pain and suffering in clinical populations.