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Cited by 138Stress Responses and CortisolTryptophan and brain disordersNeuropeptides and Animal Physiology

Effects of prior stress on LPS-induced cytokine and sickness responses

Johnson, John D., O'Connor, Kevin A., Hansen, Michael K., Watkins, Linda R., Maier, Steven F.·2003·American Journal of Physiology-Regulatory, Integrative and Comparative Physiology
DOI 10.1152/ajpregu.00230.2002
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Abstract

It has recently been reported that exposure to inescapable tailshock (IS) enhances the release of proinflammatory cytokines following bacterial challenge. However, it is not known whether the level of potentiation of proinflammatory cytokines is sufficient to exaggerate any of the physiological processes that are regulated by these cytokines. Thus, LPS was administered and fever, activity, hypothalamic-pituitary-adrenal (HPA) responses, and proinflammatory cytokine release were assessed during both the light and dark phases of the light cycle following IS. Exposure to IS resulted in elevated basal core body temperature during the light phase but not the dark phase and decreased activity during the dark phase but not the light phase. IS animals had significantly greater fever, corticosterone, and ACTH responses following LPS during both the light and dark phases, whereas enhanced proinflammatory cytokine responses were only observed during the light phase. These data suggest that enhanced proinflammatory cytokine responses are not necessary to observe enhanced HPA or fever responses.

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Crossref · 10.1152/ajpregu.00230.2002

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  • Stressors can induce a slower developing, longer lasting sensitization (priming) of neuroinflammatory responses to subsequently occurring infectious/pathogenic stimuli or stressors.

    “The second is a slower developing, longer lasting (days) sensitization (or “priming”) of neuroinflammatory responses to subsequently occurring infectious/pathogenic stimuli or stressors (i.e. delayed challenge) (Johnson et al., 2003).”

    From Stress- and Glucocorticoid-Induced Priming of Neuroinflammatory Responses: Potential Mechanisms of Stress-Induced Vulnerability to Drugs of Abuse (2011) · cites this paper as Johnson et al., 2003

  • GR signaling is essential for the cross-sensitization between stress and the inflammatory response to LPS.

    “GR signaling was thus proposed to be essential for the cross-sensitization between stress and the inflammatory response to LPS.”

    From The HPA – Immune Axis and the Immunomodulatory Actions of Glucocorticoids in the Brain (2014) · cites this paper as [142]

  • The priming effects of stress on the ensuing immune response could be abated with RU486 or by experimentally maintaining plasma GCs to basal levels in adrenalectomized animals.

    “Interestingly, in these studies the priming effects of stress (regardless of its chronicity) on the ensuing immune response could be abated with RU486 or by experimentally maintaining plasma GCs to basal levels in adrenalectomized animals.”

    From The HPA – Immune Axis and the Immunomodulatory Actions of Glucocorticoids in the Brain (2014) · cites this paper as [142]

  • Both acute and chronic stress elicit an HPA response and exacerbate salient features of inflammation in the CNS provided that they occur prior to peripheral or cerebral immune insults.

    “As a matter of act, both types of stress elicit an HPA response and were shown to exacerbate salient features of inflammation in the CNS provided that they occur prior to peripheral or cerebral immune insults.”

    From The HPA – Immune Axis and the Immunomodulatory Actions of Glucocorticoids in the Brain (2014) · cites this paper as [142]

  • Acute stressors such as inescapable tailshocks potentiate the expression of pro-inflammatory mediators in specific regions of the brain following peripheral administration of LPS in rodents.

    “For instance, acute stressors such as inescapable tailshocks (IS) were demonstrated to potentiate the expression of pro-inflammatory mediators in specific regions of the brain following the peripheral administration of LPS in rodents (140–142).”

    From The HPA – Immune Axis and the Immunomodulatory Actions of Glucocorticoids in the Brain (2014) · cites this paper as [142]

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Authors
Johnson, J. D., O'Connor, K. A., Hansen, M. K., Watkins, L. R., & Maier, S. F.
Affiliations
  • University of Colorado Boulder (US)
  • Department of Psychology and Center for Neuroscience, University of Colorado, Boulder, Colorado 80309-0345
ORCID
Venue
American Journal of Physiology-Regulatory, Integrative and Comparative Physiology
Publisher
American Physiological Society
Published
2003-02-01
Volume
284
Issue
2
Pages
R422-R432
ISSN
  • 0363-6119 (ISSN-L)
  • 1522-1490
DOI
10.1152/ajpregu.00230.2002
OpenAlex
W2002195787
Cited by
138
References
53
Citations by year
2026: 1 · 2025: 1 · 2024: 6 · 2023: 1 · 2021: 4 · 2020: 5 · 2019: 7 · 2018: 8 · 2017: 7 · 2016: 8 · 2015: 10 · 2014: 10 · 2013: 6 · 2012: 6
FWCI
2.64
Type
journal article
Language
en
Open access
closed
Locations
  • American Journal of Physiology-Regulatory, Integrative and Comparative Physiology (publishedVersion)
  • PubMed (publishedVersion)
Funders
National Institute of Mental Health (MH-0314, MH-5045, MH-1558, MH-5283)
Topics
  • Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
  • Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuropeptides and Animal Physiology
Keywords
lipopolysaccharide, inflammatory cytokines, sickness behavior, fever, hypothalamic-pituitary-adrenal axis, corticosterone, ACTH, circadian rhythm, light-dark cycle, core body temperature
MeSH terms
Adrenocorticotropic Hormone, Animals, Body Temperature, Brain, Circadian Rhythm, Fever, Hydrocortisone, Interleukin-1, Lipopolysaccharides, Male, Stress, Physiological, Time Factors, Tumor Necrosis Factor-alpha, Interleukin-6, Cytokines, Rats, Sprague-Dawley, Rats

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