Stress System Activity, Innate and T Helper Cytokines, and Susceptibility to Immune‐Related Diseases

Jul 21, 2006Annals of the New York Academy of Sciences

Stress system activity, immune signals, and risk of immune diseases

AI simplified

Circadian Biology on OpenScience ↗PubMed ↗DOI ↗

Abstract

Glucocorticoids and catecholamines, the major stress hormones, inhibit IL-12, TNF-alpha, and INF-gamma while upregulating IL-10, IL-4, and TGF-beta production.

Stress hormones may induce a Th2 shift that protects against excessive proinflammatory cytokine responses.
Under certain conditions, stress hormones can facilitate inflammation by promoting the production of proinflammatory cytokines.
Dysregulation of the balance between pro- and anti-inflammatory cytokines is linked to conditions like autoimmunity, chronic infections, and major depression.
Changes in stress system activity, such as during acute stress or pregnancy, may influence disease activity and progression.
The interaction between stress hormones and cytokine production may be a key mechanism affecting disease susceptibility and outcomes in immune-related diseases.

AI simplified

Associations between stress and health outcomes have now been carefully documented, but the mechanisms by which stress specifically influences disease susceptibility and outcome remain poorly understood. Recent evidence indicates that glucocorticoids (GCs) and catecholamines (CAs), the major stress hormones, inhibit systemically IL-12, TNF-alpha, and INF-gamma, but upregulate IL-10, IL-4, and TGF-beta production. Thus, during an immune and inflammatory response, the activation of the stress system, through induction of a Th2 shift may protect the organism from systemic "overshooting" with T helper lymphocyte 1 (Th1)/proinflammatory cytokines. In certain local responses and under certain conditions, however, stress hormones may actually facilitate inflammation, through induction of IL-1, IL-6, IL-8, IL-18, TNF-alpha, and CRP production, and through activation of the corticotropin-releasing hormone (CRH)/substance P(SP)-histamine axis. Autoimmunity, chronic infections, major depression, and atherosclerosis are characterized by a dysregulation of the pro/anti-inflammatory and Th1/Th2 cytokine balance. Thus, hyperactive or hypoactive stress system, and a dysfunctional neuroendocrine-immune interface associated with abnormalities of the "systemic anti-inflammatory feedback" and/or "hyperactivity" of the local proinflammatory factors may contribute to the pathogenesis of these diseases. Conditions that are associated with significant changes in stress system activity, such as acute or chronic stress, cessation of chronic stress, pregnancy and the postpartum period, or rheumatoid arthritis (RA) through modulation of the systemic or local pro/anti-inflammatory and Th1/Th2 cytokine balance, may suppress or potentiate disease activity and/or progression. Thus, stress hormones-induced inhibition or upregulation of innate and Th cytokine production may represent an important mechanism by which stress affects disease susceptibility, activity, and outcome of various immune-related diseases.

Full Text

Full text is available at the source.

View full text ↗

Stress System Activity, Innate and T Helper Cytokines, and Susceptibility to Immune‐Related Diseases

Abstract

Full Text

You found one interesting study. We’ll send the next 7.

what lands in your inbox each week:

Recent issues from the circadian biology brief

Abstract

Full Text

Related papers

You found one interesting study. We’ll send the next 7.

what lands in your inbox each week:

Recent issues from the circadian biology brief