Mind-body interactions in the regulation ...
Document type :
Article dans une revue scientifique: Article original
PMID :
Permalink :
Title :
Mind-body interactions in the regulation of airway inflammation in asthma: A PET study of acute and chronic stress.
Author(s) :
Rosenkranz, Melissa A [Auteur]
Esnault, Stéphane [Auteur]
University of Wisconsin School of Medicine and Public Health
Christian, Bradley T [Auteur]
Crisafi, Gina [Auteur]
Gresham, Lauren K [Auteur]
Higgins, Andrew T [Auteur]
Moore, Mollie N [Auteur]
Moore, Sarah M [Auteur]
Weng, Helen Y [Auteur]
Salk, Rachel H [Auteur]
Busse, William W [Auteur]
Davidson, Richard J [Auteur]
Esnault, Stéphane [Auteur]
University of Wisconsin School of Medicine and Public Health
Christian, Bradley T [Auteur]
Crisafi, Gina [Auteur]
Gresham, Lauren K [Auteur]
Higgins, Andrew T [Auteur]
Moore, Mollie N [Auteur]
Moore, Sarah M [Auteur]
Weng, Helen Y [Auteur]
Salk, Rachel H [Auteur]
Busse, William W [Auteur]
Davidson, Richard J [Auteur]
Journal title :
Brain, Behavior, and Immunity
Abbreviated title :
Brain Behav Immun
Volume number :
58
Pages :
18-30
Publication date :
2016-11-01
ISSN :
1090-2139
English keyword(s) :
Adult
Amylases
Asthma
Brain
Female
Humans
Hydrocortisone
Inflammation
Male
Pneumonia
Positron-Emission Tomography
Respiratory Function Tests
Stress, Psychological
Young Adult
ACC
Asthma
Cortisol
IL-1
IL-17
Inflammation
Insula
PET
Stress
TSST
Amylases
Asthma
Brain
Female
Humans
Hydrocortisone
Inflammation
Male
Pneumonia
Positron-Emission Tomography
Respiratory Function Tests
Stress, Psychological
Young Adult
ACC
Asthma
Cortisol
IL-1
IL-17
Inflammation
Insula
PET
Stress
TSST
HAL domain(s) :
Sciences du Vivant [q-bio]
English abstract : [en]
Psychological stress has long been recognized as a contributing factor to asthma symptom expression and disease progression. Yet, the neural mechanisms that underlie this relationship have been largely unexplored in research ...
Show more >Psychological stress has long been recognized as a contributing factor to asthma symptom expression and disease progression. Yet, the neural mechanisms that underlie this relationship have been largely unexplored in research addressing the pathophysiology and management of asthma. Studies that have examined the mechanisms of this relationship in the periphery suggest that it is the superimposition of acute stress on top of chronic stress that is of greatest concern for airway inflammation. We compared asthmatic individuals with high and low levels of chronic life stress in their neural and peripheral physiological responses to the Trier Social Stress Test and a matched control task. We used FDG-PET to measure neural activity during performance of the two tasks. We used both circulating and airway-specific markers of asthma-related inflammation to assess the impact of acute stress in these two groups. Asthmatics under chronic stress had a larger HPA-axis response to an acute stressor, which failed to show the suppressive effects on inflammatory markers observed in those with low chronic stress. Moreover, our PET data suggest that greater activity in the anterior insula during acute stress may reflect regulation of the effect of stress on inflammation. In contrast, greater activity in the mid-insula and perigenual anterior cingulate seems to reflect greater reactivity and was associated with greater airway inflammation, a more robust alpha amylase response, and a greater stress-induced increase in proinflammatory cytokine mRNA expression in airway cells. Acute stress is associated with increases in markers of airway inflammation in asthmatics under chronic stress. This relationship may be mediated by interactions between the insula and anterior cingulate cortex, that determine the salience of environmental cues, as well as descending regulatory influence of inflammatory pathways in the periphery.Show less >
Show more >Psychological stress has long been recognized as a contributing factor to asthma symptom expression and disease progression. Yet, the neural mechanisms that underlie this relationship have been largely unexplored in research addressing the pathophysiology and management of asthma. Studies that have examined the mechanisms of this relationship in the periphery suggest that it is the superimposition of acute stress on top of chronic stress that is of greatest concern for airway inflammation. We compared asthmatic individuals with high and low levels of chronic life stress in their neural and peripheral physiological responses to the Trier Social Stress Test and a matched control task. We used FDG-PET to measure neural activity during performance of the two tasks. We used both circulating and airway-specific markers of asthma-related inflammation to assess the impact of acute stress in these two groups. Asthmatics under chronic stress had a larger HPA-axis response to an acute stressor, which failed to show the suppressive effects on inflammatory markers observed in those with low chronic stress. Moreover, our PET data suggest that greater activity in the anterior insula during acute stress may reflect regulation of the effect of stress on inflammation. In contrast, greater activity in the mid-insula and perigenual anterior cingulate seems to reflect greater reactivity and was associated with greater airway inflammation, a more robust alpha amylase response, and a greater stress-induced increase in proinflammatory cytokine mRNA expression in airway cells. Acute stress is associated with increases in markers of airway inflammation in asthmatics under chronic stress. This relationship may be mediated by interactions between the insula and anterior cingulate cortex, that determine the salience of environmental cues, as well as descending regulatory influence of inflammatory pathways in the periphery.Show less >
Language :
Anglais
Peer reviewed article :
Oui
Audience :
Internationale
Popular science :
Non
Administrative institution(s) :
Université de Lille
Inserm
CHU Lille
Inserm
CHU Lille
Collections :
Submission date :
2023-10-23T15:19:59Z
2024-03-16T08:42:08Z
2024-03-16T08:42:08Z
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