Regional cerebral glucose metabolism in the insula during acute stress predicts increased post-stress pulmonary inflammation in asthma

Although psychological factors contribute to the frequency, severity, and burden of asthma symptoms, the role of the brain in the pathophysiology and treatment of this disease is largely unknown. To examine the neural mechanisms which may regulate airway inflammation in asthma, we used [18F]fluoro-deoxyglucose positron emission tomography (FDG-PET) to identify neural circuits that are active during performance of a social stress task or a matched control condition. Asthmatic subjects with either high or low levels of chronic life stress underwent both stress and control conditions. Fractional exhaled nitric oxide (FeNO) was collected at baseline, as well as hourly post-challenge, and provided a measure of airway inflammation. These data reveal that, in those with high levels of chronic stress, an acute stressor leads to elevated post-stress FeNO levels relative to those with low chronic stress. In addition, increased regional glucose metabolism in the insular cortex predicts overall FeNO levels. This region of the insula is nearly identical to a region we identified in a previous study where activation following challenge with inhaled allergen predicted the increase in percentage of eosinophils in lung tissue 24 h later. These data corroborate previous evidence indicating a role for the insula in the interaction of emotion and inflammation in asthma and may lead to novel targets for future treatment.