Neuropsychiatry phenotype in asthma: Psychological stress-induced alterations of the neuroendocrine-immune system in allergic airway inflammation

Allergol Int. 2017 Sep;66S:S2-S8. doi: 10.1016/j.alit.2017.06.005. Epub 2017 Jun 29.


Since the recognition of asthma as a syndrome with complex pathophysiological signs and symptoms, recent research has sought to classify asthma phenotypes based on its clinical and molecular pathological features. Psychological stress was first recognized as a potential immune system modulator of asthma at the end of the 19th century. The activation of the central nervous system (CNS) upon exposure to psychological stress is integral for the initiation of signal transduction processes. The stress hormones, including glucocorticoids, epinephrine, and norepinephrine, which are secreted following CNS activation, are involved in the immunological alterations involved in psychological stress-induced asthma exacerbation. The mechanisms underlying this process may involve a pathological series of events from the brain to the lungs, which is attracting attention as a conceptually advanced phenotype in asthma pathogenesis. This review presents insights into the critical role of psychological stress in the development and exacerbation of allergic asthma, with a special focus on our own data that emphasizes on the continuity from the central sensing of psychological stress to enhanced eosinophilic airway inflammation.

Keywords: Bronchial asthma; Glucocorticoids; Opioid receptors; Psychological stress; Type 2 T helper.

Publication types

  • Review

MeSH terms

  • Animals
  • Asthma / etiology*
  • Asthma / metabolism
  • Asthma / psychology*
  • Brain / immunology
  • Brain / metabolism
  • Brain / physiopathology
  • Disease Progression
  • Endocrine System
  • Hormones / metabolism
  • Humans
  • Inflammation / etiology
  • Inflammation / metabolism
  • Neuroimmunomodulation
  • Neuropsychological Tests
  • Phenotype*
  • Stress, Psychological
  • Th2 Cells / immunology
  • Th2 Cells / metabolism


  • Hormones