A pre-conditioning stress accelerates increases in mouse plasma inflammatory cytokines induced by stress

Research output: Contribution to journalArticle

17 Citations (Scopus)

Abstract

Background: Major depressive disorder is a prevalent disease that is inadequately treated with currently available interventions. Stress increases susceptibility to depression in patients and rodent models. Depression is also associated with aberrant activation of inflammation, such as increases in circulating levels of interleukin (IL)-1β, IL-6, and tumor necrosis factor-α (TNFα). The two main goals of this study were (i) to identify cytokine changes measuring a broad panel of 19 cytokines, and (ii) to test if a pre-conditioning stress altered the inflammatory response to a subsequent stress. Result: Stress-induced changes in mouse plasma cytokines were measured by multiplex following administration of one or two daily stresses of inescapable foot shocks using the learned helplessness paradigm for modeling depression-like behavior. Conclusions: Acute stress broadly activates inflammation in mice, and the inflammatory response is more rapid following repeated stress, actions that may contribute to deleterious effects of stress on depression and other stress-linked diseases.

Original languageEnglish (US)
Article number31
JournalBMC Neuroscience
Volume16
Issue number1
DOIs
StatePublished - May 7 2015

Fingerprint

Depression
Cytokines
Learned Helplessness
Inflammation
Major Depressive Disorder
Interleukin-1
Foot
Rodentia
Shock
Interleukin-6
Tumor Necrosis Factor-alpha
Conditioning (Psychology)

Keywords

  • Cytokines
  • Depression
  • Inflammation
  • Pre-conditioning
  • Stress
  • Tumor necrosis factor-α

ASJC Scopus subject areas

  • Neuroscience(all)
  • Cellular and Molecular Neuroscience

Cite this

A pre-conditioning stress accelerates increases in mouse plasma inflammatory cytokines induced by stress. / Cheng, Yuyan; Jope, Richard S; Beurel, Eleonore.

In: BMC Neuroscience, Vol. 16, No. 1, 31, 07.05.2015.

Research output: Contribution to journalArticle

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