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Stress as a risk factor in the pathogenesis of rheumatoid arthritis.

Authors
  • Cutolo, Maurizio
  • Straub, Rainer H
Type
Published Article
Journal
Neuroimmunomodulation
Publication Date
Jan 01, 2006
Volume
13
Issue
5-6
Pages
277–282
Identifiers
PMID: 17709949
Source
Medline
License
Unknown

Abstract

Stress is now recognized as an important risk factor in the pathogenesis of autoimmune rheumatic diseases (i.e. rheumatoid arthritis) by considering that the activation of the stress response system influences the close relationships existing between the hypothalamic-pituitary-adrenal axis, the sympathetic nervous system and the immune system. The stress response results in the release of neurotransmitters (norepinephrine), hormones (cortisol) and immune cells which serve to send an efferent message from the brain to the periphery. Major life events lead to an intense release of stress mediators (large time integral of released neurotransmitters and hormones), whereas in minor life events, only short-lived surges of neurotransmitters and hormones are expected. Therefore, it is suggested that neurotransmitters such as norepinephrine or stress hormones such as cortisol might have different effects on immune/inflammatory responses at high and low concentrations present during short or extended periods of time, respectively. Long-lasting (chronic) stress may lead to proinflammatory effects because no adequate long-term responses of stress axes (anti-inflammatory) are to be expected.

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