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Cited by 270Stress Responses and CortisolTryptophan and brain disordersImmune Response and Inflammation

Prior Stressor Exposure Sensitizes LPS-Induced Cytokine Production

Johnson, John D., O'Connor, Kevin A., Deak, Terrence, Stark, Matt, Watkins, Linda R., Maier, Steven F.·2002·Brain, Behavior, and Immunity
DOI 10.1006/brbi.2001.0638
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Abstract

Exposure to stressors often alters the subsequent responsiveness of many systems. The present study tested whether prior exposure to inescapable tailshock (IS) alters the interleukin (IL)-1beta, tumor necrosis factor (TNF)-alpha, or IL-6 response to an injection of bacterial endotoxin (lipopolysaccharide; LPS). Rats were exposed to IS or remained as home cage controls (HCC); 24 h later animals were injected i.p. with either 10 microg/kg LPS or equilvolume sterile saline. IS significantly increased plasma TNF-alpha, IL-1beta, and pituitary, hypothalamus, hippocampus, cerebellum IL-1beta 1 h, but not 2 h, after LPS, compared to controls. Additional animals were injected with LPS or saline 4, 10, or 21 days after exposure to IS and tail vein blood was collected and assayed for IL-1beta. An enhanced plasma IL-1beta response occurred 4 days after IS, but was gone by 10 days. These results suggest that exposure to IS sensitizes the innate immune response to LPS by resulting in either a larger or a more rapid induction of proinflammatory cytokines.

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Crossref · 10.1006/brbi.2001.0638

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89 of 89 references verified0 citation errors · 0 not checkable

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  • Stress and depression can permanently alter the responsiveness of the immune system.

    “Stress and depression can permanently alter the responsiveness of the immune system (41-44).”

    From Chronic stress and age-related increases in the proinflammatory cytokine IL-6. (2003) · cites this paper as [41]

  • Prior stressor exposure appears to prime proinflammatory cytokine responses, such that subsequent exposure to lipopolysaccharide resulted in larger or more rapid induction of proinflammatory cytokines in stressed rats compared with nonstressed controls.

    “For example, prior stressor exposure appears to prime proinflammatory cytokine responses, such that subsequent exposure to a bacterial endotoxin, lipopolysaccharide, resulted in a larger or more rapid induction of proinflammatory cytokines in stressed rats compared with nonstressed controls (41).”

    From Chronic stress and age-related increases in the proinflammatory cytokine IL-6. (2003) · cites this paper as [41]

  • In healthy participants, serum concentrations of lipocalin-type PGD synthase vary throughout the day, with highest levels at night and lowest in the afternoon; total sleep deprivation blunted the nocturnal increase and elevated daytime levels.

    “serum concentrations of lipocalin-type PGD synthase, which catalyzes the conversion from PGH2 to PGD2, have been reported to vary throughout the day, with highest levels at night (sleep period) and lowest levels in the afternoon. Total sleep deprivation blunted the nocturnal increase at night and elevated levels during the daytime (275)”

    From The Sleep-Immune Crosstalk in Health and Disease (2019) · cites this paper as [275]

  • In the periphery, acute stress 24 hr prior to LPS treatment augments LPS-induced increases in plasma levels of IL-1β, TNF-α, and IL-6.

    “For example, acute stress 24 hr prior to lipopolysaccharide (LPS) treatment augments LPS-induced increases in plasma levels of IL-1β, TNF-α, and IL-6 (Johnson et al., 2002).”

    From The Stressed CNS: When Glucocorticoids Aggravate Inflammation (2009) · cites this paper as Johnson et al., 2002

  • 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 [141]

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Authors
Johnson, J. D., O'Connor, K. A., Deak, T., Stark, M., Watkins, L. R., & Maier, S. F.
Affiliations
University of Colorado Boulder (US)
ORCID
Venue
Brain, Behavior, and Immunity
Publisher
Elsevier BV
Published
2002-08
Volume
16
Issue
4
Pages
461-476
ISSN
0889-1591 (ISSN-L)
DOI
10.1006/brbi.2001.0638
OpenAlex
W2148779404
Cited by
270
References
91
Citations by year
2026: 5 · 2025: 1 · 2024: 8 · 2023: 5 · 2022: 3 · 2021: 5 · 2020: 6 · 2019: 12 · 2018: 14 · 2017: 17 · 2016: 12 · 2015: 21 · 2014: 20 · 2013: 14 · 2012: 12
FWCI
4.81
Type
journal article
Language
en
Open access
closed
Licence
Locations
  • Brain Behavior and Immunity (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health
  • 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 › Immunology and Microbiology › Immunology › Immune Response and Inflammation
Keywords
lipopolysaccharide, endotoxin, IL-1β, TNF-α, interleukin-6, inflammatory cytokines, innate immune response, stress-immune interaction, hippocampus, hypothalamus, pituitary gland, rats
MeSH terms
Animals, Brain, Electroshock, Interleukin-1, Lipopolysaccharides, Male, Stress, Physiological, Time Factors, Tumor Necrosis Factor-alpha, Interleukin-6, Cytokines, Rats, Sprague-Dawley, Rats

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