Are There Neurophenotypes for Asthma? Functional Brain Imaging of the Interaction between Emotion and Inflammation in Asthma

Abstract

BackgroundAsthma is a chronic inflammatory disease noteworthy for its vulnerability to stress and emotion-induced symptom intensification. The fact that psychological stress and mood and anxiety disorders appear to increase expression of asthma symptoms suggests that neural signaling between the brain and lung at least partially modulates the inflammatory response and lung function. However, the precise nature of the neural pathways implicated in modulating asthma symptoms is unknown. Moreover, the extent to which variations in neural signaling predict different phenotypes of disease expression has not been studied.Methods and ResultsWe used functional magnetic resonance imaging to measure neural signals in response to asthma-specific emotional cues, following allergen exposure, in asthmatics with a dual response to allergen challenge (significant inflammation), asthmatics with only an immediate response (minimal inflammation), and healthy controls. The anterior insular cortex was differentially activated by asthma-relevant cues, compared to general negative cues, during the development of the late phase of the dual response in asthmatics. Moreover, the degree of this differential activation predicted changes in airway inflammation.ConclusionsThese findings indicate that neurophenotypes for asthma may be identifiable by neural reactivity of brain circuits known to be involved in processing emotional information. Those with greater activation in the anterior insula, in response to asthma-relevant psychological stimuli, exhibit greater inflammatory signals in the lung and increased severity of disease and may reflect a subset of asthmatics most vulnerable to the development of psychopathology. This approach offers an entirely new target for potential therapeutic intervention in asthma.

Risk of developing major depression and bipolar disorder among adolescents with atopic diseases: A nationwide longitudinal study in Taiwan

“…In addition, the additive effect of atopic comorbidities in the inflammatory dysregulation may explain the dose-dependent relationship between a greater number of atopic comorbidities and a higher likelihood of subsequent depression and bipolar disorder. Finally, functional neuroimaging studies also supported the existence of this comorbidity between atopy and mood disorders (Rosenkranz et al, 2005;Ishiuji et al, 2009;Rosenkranz et al, 2012). Using functional magnetic resonance imaging, Ishiuji et al found that patients with atopic dermatitis exhibited bilateral activation of the anterior cingulate cortex (ACC), posterior cingulate cortex (PCC), and dorsolateral prefrontal cortex (DLPFC) (Ishiuji et al, 2009).…”

Stress and Bronchodilator Response in Children with Asthma

“…Such connectivity may also be directly linked to airway inflammation in asthma. In a previous study, individuals with atopic asthma who were exposed to allergens had differential activation of the anterior insula by asthma-relevant emotional cues during the late phase of the dual response, and this differential activation was associated with airway inflammation (62).…”

The Involvement of Glucocorticoids in Psychological Stress-Induced Exacerbations of Experimental Allergic Asthma

“…It will be necessary to further explore the cellular and molecular events linking the corticosterone release to stress-induced immune regulation accelerating Th2-driven adaptive immunity. These investigations would further clarify the pathological role of the neuroendocrine-immune axis in psychological stress-related asthma exacerbation, leading to the development of new strategies for the treatment of specific asthma phenotypes such as psychiatry-related asthma [46,47]. …”