Cited by 128Stress Responses and CortisolNeuroinflammation and Neurodegeneration MechanismsAdrenal Hormones and Disorders

The DOI matches its Crossref record; 43 of the 47 references it cites were found in a registry or an index.

Adrenalectomy enhances pro-inflammatory cytokines gene expression, in the spleen, pituitary and brain of mice in response to lipopolysaccharide

Abstract

To assess the possible influence of endogenous glucocorticoids on cytokine expression in the brain, adrenalectomized mice and sham operated mice were injected with saline or lipopolysaccharide (LPS, 10 micrograms/mouse, subcutaneously) and the levels of transcripts for IL-1 alpha, IL-1 beta, IL-1ra, IL-6 and tumor necrosis factor-alpha (TNF alpha) were determined 2 h after treatment in the spleen, pituitary, hypothalamus, hippocampus and striatum, using semi-quantitative reverse transcription polymerase chain reaction (RT-PCR). Levels of IL-1 beta were measured by ELISA in plasma and tissues of mice sacrificed after the administration of LPS or saline. LPS induced the expression of pro-inflammatory cytokines at the mRNA level in all tissues under investigation, except for TNF alpha in the hippocampus. This effect was potentiated by adrenalectomy in the spleen for IL-1 alpha and IL-1ra, the pituitary for cytokines other than IL-1ra, the hypothalamus for all cytokines, the hippocampus for cytokines other than TNF alpha, and the striatum for IL-1 alpha and IL-6. In saline-treated mice, adrenalectomy increased IL-1 alpha and IL-1 beta gene expression in the hypothalamus and IL-1 alpha gene expression in the hippocampus and striatum. LPS increased plasma and tissue levels of IL-1 beta, as determined by ELISA, and this effect was potentiated by adrenalectomy in plasma and tissues other than the spleen. These results can be interpreted to suggest that endogenous glucocorticoids regulate the neural components of the host response to infection and inflammation by inhibiting cytokine expression in peripheral organs and the brain.

Overview

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Crossref · 10.1016/0169-328x(95)00242-k

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Research works printed but not linked: 1

  1. Schöbitz, 1993, Regulation of interleukin-6 in rat, Endocrinology, 132, 1569, 10.1210/en.132.4.1569 · DOI

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Metadata

Authors
Goujon, E., Parnet, P., Layé, S., Combe, C., & Dantzer, R.
Affiliations
Inserm (FR)
Corresponding author
Dantzer, Robert
Venue
Molecular Brain Research
Publisher
Elsevier BV
Published
1996-02
Volume
36
Issue
1
Pages
53-62
ISSN
0169-328X (ISSN-L)
OpenAlex
W2010946024
Cited by
128
References
47
Citations by year
2026: 1 · 2024: 1 · 2022: 1 · 2021: 2 · 2020: 2 · 2019: 7 · 2018: 1 · 2017: 2 · 2016: 2 · 2015: 3 · 2014: 2 · 2013: 2 · 2012: 7
FWCI
3.85
Type
journal article
Language
en
Open access
closed
Locations
  • Molecular Brain Research (publishedVersion)
  • PubMed (publishedVersion)
  • HAL (submittedVersion)
Topics
  • Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adrenal Hormones and Disorders
Keywords
adrenalectomy, endogenous glucocorticoids, inflammatory cytokines, lipopolysaccharide, IL-1α, IL-1β, interleukin-1 receptor antagonist, interleukin-6, TNF-α, hypothalamus, hippocampus, striatum, pituitary gland, spleen, neuroimmune regulation, inflammation, infection
MeSH terms
Adrenal Glands, Adrenalectomy, Animals, Base Sequence, Brain, Corticosterone, Gene Expression Regulation, Inflammation, Interleukins, Lipopolysaccharides, Male, Mice, Inbred ICR, Molecular Sequence Data, Pituitary Gland, Spleen, Tumor Necrosis Factor-alpha, Cytokines, Mice

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