Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
8736263 | Allergology International | 2018 | 11 Pages |
Abstract
Psychological stress is recognized as a key factor in the exacerbation of allergic asthma, whereby brain responses to stress act as immunomodulators for asthma. In particular, stress-induced enhanced type 2 T-helper (Th2)-type lung inflammation is strongly associated with asthma pathogenesis. Psychological stress leads to eosinophilic airway inflammation through activation of the hypothalamic-pituitary-adrenal pathway and autonomic nervous system. This is followed by the secretion of stress hormones into the blood, including glucocorticoids, epinephrine, and norepinephrine, which enhance Th2 and type 17 T-helper (Th17)-type asthma profiles in humans and rodents. Recent evidence has shown that a defect of the μ-opioid receptor in the brain along with a defect of the peripheral glucocorticoid receptor signaling completely disrupted stress-induced airway inflammation in mice. This suggests that the stress response facilitates events in the central nervous and endocrine systems, thus exacerbating asthma. In this review, we outline the recent findings on the interplay between stress and neuroendocrine activities followed by stress-induced enhanced Th2 and Th17 immune responses and attenuated regulatory T (Treg) cell responses that are closely linked with asthma exacerbation. We will place a special focus on our own data that has emphasized the continuity from central sensing of psychological stress to enhanced eosinophilic airway inflammation. The mechanism that modulates psychological stress-induced exacerbation of allergic asthma through neuroendocrine activities is thought to involve a series of consecutive pathological events from the brain to the lung, which implies there to be a “neuropsychiatry phenotype” in asthma.
Keywords
NPYTLRpro-opiomelanocortinTregSNSTh17ADCYAP1R1NLRP3BALNOD2Th1Th2POMCSLITβ2ARType 2 T helperBLNbronchial lymph nodeSAMβ-ENDNucleotide-binding oligomerization domain 2CRHMORACTHACCβ-endorphinμ-Opioid receptorEndomorphinSublingual immunotherapyimmunoglobulin interleukintumor necrosis factor-αToll-like receptorcluster of differentiationAutonomic nervous systemCNSANSsympathetic nervous systemcentral nervous systemParasympathetic nervous systempituitary-adrenal systemTNF-αPsychological stressanterior cingulate cortexbronchoalveolar lavageRegulatory T lymphocytesPVNRegulatory T HPAwild typeparaventricular nucleusadrenocorticotropic hormonecorticotrophin-releasing hormonehypothalamic-pituitary-adrenalPNSGlucocorticoidsβ2-adrenergic receptorOpioid receptorsHistamine receptorglucocorticoid receptorNeuropeptide Y
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Authors
Tomomitsu Miyasaka, Kaori Dobashi-Okuyama, Tomoko Takahashi, Motoaki Takayanagi, Isao Ohno,