78. Increased glucose metabolism during acute stress in emotional neural circuitry, assessed with FDG-PET, predicts airway inflammation and psychological symptoms in asthma

Although psychological stress contributes to frequency, severity, and burden of asthma symptoms, the role of the brain in the pathophysiology and treatment of this disease is unknown. To examine the neural mechanisms through which stress contributes to airway inflammation, asthmatic subjects high or low in chronic life stress underwent an acute stressor. [18F]Fluoro-deoxyglucose positron emission tomography (FDG-PET) was used to identify neural circuits active during performance of a social stress task or a matched control condition. Sputum was collected to assess markers of airway inflammation, including expression of genes in the IL-17 pathway, products of which can contribute to both inflammation and depression. Preliminary results indicate that, during an acute stressor, activation in the anterior and mid-cingulate cortex, as well as the inferior frontal gyrus is greater in those with high vs. low chronic stress. These increases in regional glucose metabolism also predicted increased gene expression in the IL-17 pathway, as well as symptoms of anxiety and depression. Moreover, those subjects high in chronic stress showed increased gene expression in the IL-17 pathway following an acute stressor, as well as increased symptoms of anxiety and depression, relative to those with low chronic stress levels. These data suggest potential neural pathways through which psychological stress may influence airway inflammation, thus leading to an increase in asthma symptoms, disease severity, and uncovering novel targets for future treatment.