The DOI matches its Crossref record; 87 of the 91 references it cites were found in a registry or an index.
Prior Stressor Exposure Sensitizes LPS-Induced Cytokine Production
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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In the citing paper
“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]
In the citing paper
“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 the citing paper
“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 citing paper
“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
In the citing paper
“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]
In the citing paper
“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 [141]
In the citing paper
“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 [141]
In the citing paper
“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 [141]
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Metadata
- Authors
- Johnson, J. D., O'Connor, K. A., Deak, T., Stark, M., Watkins, L. R., & Maier, S. F.
- Affiliations
- University of Colorado Boulder (US)
- Venue
- Brain, Behavior, and Immunity
- Publisher
- Elsevier BV
- Published
- 2002-08
- Volume
- 16
- Issue
- 4
- Pages
- 461-476
- ISSN
- 0889-1591 (ISSN-L)
- 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
- 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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