Peripheral and central proinflammatory cytokine response to a severe acute stressor

O'Connor, Kevin A; Johnson, John D; Hansen, Michael K; Wieseler Frank, Julie L; Maksimova, Elena; Watkins, Linda R; Maier, Steven F

doi:10.1016/j.brainres.2003.08.006

Cited by 247Stress Responses and CortisolTryptophan and brain disordersNeuroinflammation and Neurodegeneration Mechanisms

Peripheral and central proinflammatory cytokine response to a severe acute stressor

O'Connor, Kevin A, Johnson, John D, Hansen, Michael K, Wieseler Frank, Julie L, Maksimova, Elena, Watkins, Linda R, Maier, Steven F·2003·Brain Research

DOI 10.1016/j.brainres.2003.08.006

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Abstract

The role of proinflammatory cytokines in the response to acute stressor exposure has received recent attention. Exposure to a single session of inescapable shock (IS) induces peripheral and central proinflammatory cytokines. Other stressors also increase expression of proinflammatory cytokine mRNA and/or protein in various tissues. However, the induction of central and peripheral proinflammatory cytokines by stressors remains controversial and the pattern of cytokine induction is not consistent across stressors. The present experiments sought to examine the pattern of the proinflammatory cytokine response to a stressor known to cause elevations of IL-1beta protein. mRNA expression for three proinflammatory cytokines, IL-1beta, TNF-alpha and IL-6, and IL-1beta protein was examined after IS. IS increases IL-1beta mRNA and/or protein in a variety of tissues, including hypothalamus, hippocampus, pituitary and spleen. Furthermore, IS concomitantly alters IL-1beta mRNA and protein in hypothalamus and spleen, while the IL-1beta mRNA increase in pituitary lags behind the increase of IL-1beta protein. Interestingly, IL-1beta mRNA is elevated in hippocampus 4 h after IS, but an increase of IL-1beta protein in hippocampus is not detected. Expression of TNF-alpha and IL-6 mRNA do not increase in response to IS. Indeed, TNF-alpha mRNA expression decreases in cortex, pituitary and liver immediately after IS. These findings suggest that alterations of proinflammatory cytokine expression by stressors, and IS in particular, are region- and cytokine-specific.

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Authors: O'Connor, K. A., Johnson, J. D., Hansen, M. K., Wieseler Frank, J. L., Maksimova, E., Watkins, L. R., & Maier, S. F.
Affiliations: University of Colorado Boulder (US)
Corresponding author: O'Connor, Kevin A
ORCID: Hansen, Michael K
Watkins, Linda R
Maier, Steven F
Venue: Brain Research
Publisher: Elsevier BV
Published: 2003-11
Volume: 991
Issue: 1-2
Pages: 123-132
ISSN: 0006-8993 (ISSN-L)
DOI: 10.1016/j.brainres.2003.08.006
OpenAlex: W2093539486
Cited by: 247
References: 43
Citations by year: 2026: 4 · 2025: 2 · 2024: 3 · 2023: 4 · 2022: 7 · 2021: 10 · 2020: 6 · 2019: 15 · 2018: 7 · 2017: 9 · 2016: 14 · 2015: 12 · 2014: 13 · 2013: 11 · 2012: 11
FWCI: 3.64
Type: journal article
Language: en
Open access: closed
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations: Brain Research (publishedVersion)
PubMed (publishedVersion)
Funders: National Institutes of Health (5r01mh045045-12, 5r01mh055283-05)
National Institute of Mental Health (MH 01558, MH55283, MH-00314, MH-45045)
Topics: Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords: inflammatory cytokines, acute stress, inescapable shock, IL-1β, TNF-α, interleukin-6, hypothalamus, hippocampus, pituitary gland, spleen, stress-induced inflammation
MeSH terms: Animals, Brain, Electroshock, Enzyme-Linked Immunosorbent Assay, Interleukin-1, Male, RNA, Messenger, Stress, Psychological, Time Factors, Tumor Necrosis Factor-alpha, Interleukin-6, Gene Expression, Cytokines, Rats, Sprague-Dawley, Peripheral Nervous System, Reverse Transcriptase Polymerase Chain Reaction, Rats

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Peripheral and central proinflammatory cytokine response to a severe acute stressor

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