Effect of acute systemic inflammatory response and cytokines on the transcription of the genes encoding cyclooxygenase enzymes (COX-1 and COX-2) in the rat brain.

Lacroix, Steve; Rivest, Serge

doi:10.1046/j.1471-4159.1998.70020452.x

Cited by 280Inflammatory mediators and NSAID effectsNeuroinflammation and Neurodegeneration MechanismsPain Mechanisms and Treatments

Effect of acute systemic inflammatory response and cytokines on the transcription of the genes encoding cyclooxygenase enzymes (COX-1 and COX-2) in the rat brain.

Lacroix, Steve, Rivest, Serge·1998·Journal of Neurochemistry

DOI 10.1046/j.1471-4159.1998.70020452.x

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Abstract

The aim of this study was to investigate the influence of the acute-phase response and the proinflammatory cytokines on the transcription of the genes encoding the limiting enzymes for the production of prostaglandins, cyclooxygenase (COX)-1 and COX-2, in the rat brain. The bacterial endotoxin lipopolysaccharide (intravenous and intraperitoneal) and turpentine (intramuscular) were used as different models of inflammation in adult male rats. Animals were also killed at various times after intravenous administration of interleukin-1beta, tumor necrosis factor-alpha, and interleukin-6, and mRNAs encoding COX-1 and COX-2 were assayed by in situ hybridization histochemistry. A profound transcriptional activation of the gene encoding COX-2 was detected over blood vessels of the entire brain microvasculature, choroid plexus, and leptomeninges of lipopolysaccharide-challenged rats. Injection of the endotoxin intravenously also increased COX-2 gene expression within parvocellular division of the hypothalamic paraventricular nucleus. It is interesting that intramuscular turpentine injection stimulated transcription of COX-2 along endothelium of brain capillaries, and the signal of this transcript paralleled the inflammation of the left hind limb. A robust COX-2 mRNA signal was detected rapidly in the brain microvessels of interleukin-1beta-injected rats, whereas tumor necrosis factor-alpha administration caused a modest but significant induction of this transcript. In contrast, intravenous injection of interleukin-6 did not alter genetic expression of COX-2, and none of the above described models affected the synthesis of COX-1 gene in the rat brain. These results indicate that specific cell populations, in particular vascular- and/or perivascular-associated cells, are responsible for the central production of prostaglandins during systemic inflammation, and circulating interleukin-1beta is likely to be a potent mediator of this response.

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In the latter study, IL-6 did not induce COX-2 expression.
“However, in this latter study IL-6 did not induce COX-2 expression.”
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Induction by lipopolysaccharide of cyclooxygenase-2 mRNA in rat brain; its possible role in the febrile response
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An Essential Role of Interleukin-1β in Mediating NF-κB Activity and COX-2 Transcription in Cells of the Blood–Brain Barrier in Response to a Systemic and Localized Inflammation But Not During Endotoxemia
Laflamme, N., Lacroix, S., & Rivest, S. (1999) · Journal of Neuroscience · doi:10.1523/jneurosci.19-24-10923.1999 · Cited by 287 · see citing works
Endothelial cells of the rat brain vasculature express cyclooxygenase-2 mRNA in response to systemic interleukin-1β: a possible site of prostaglandin synthesis responsible for fever
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Authors: Lacroix, S., & Rivest, S.
Affiliations: Centre hospitalier de l'Université Laval (CA)
Corresponding author: Rivest, Serge
ORCID: Lacroix, Steve
Rivest, Serge
Venue: Journal of Neurochemistry
Publisher: Wiley
Published: 1998-02
Volume: 70
Issue: 2
Pages: 452-466
ISSN: 0022-3042 (ISSN-L)
1471-4159
DOI: 10.1046/j.1471-4159.1998.70020452.x
OpenAlex: W2063310609
Cited by: 280
References: 70
Citations by year: 2025: 1 · 2024: 4 · 2023: 3 · 2022: 6 · 2021: 6 · 2020: 3 · 2019: 2 · 2018: 3 · 2017: 4 · 2016: 6 · 2015: 5 · 2014: 5 · 2013: 12 · 2012: 5
FWCI: 17.58
Type: journal article
Language: en
Open access: closed
Licence: onlinelibrary.wiley.com/termsAndConditions#vor (vor, 1747 d)
Locations: Journal of Neurochemistry (publishedVersion)
PubMed (publishedVersion)
Topics: Health Sciences › Medicine › Pharmacology › Inflammatory mediators and NSAID effects
Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Health Sciences › Medicine › Physiology › Pain Mechanisms and Treatments
Keywords: cyclooxygenase-2, cyclooxygenase-1, acute systemic inflammation, inflammatory cytokines, IL-1β, TNF-α, interleukin-6, lipopolysaccharide, turpentine, prostaglandin synthesis, cerebral microvasculature, choroid plexus, paraventricular nucleus, hypothalamus, gene transcription, neuroinflammation
MeSH terms: Acute Disease, Animals, Brain, Escherichia coli, Humans, Inflammation, Injections, Intramuscular, Injections, Intraperitoneal, Injections, Intravenous, Interleukin-1, Isoenzymes, Lipopolysaccharides, Male, Membrane Proteins, Paraventricular Hypothalamic Nucleus, Prostaglandin-Endoperoxide Synthases, Recombinant Proteins, RNA, Messenger, Transcription, Genetic, Tumor Necrosis Factor-alpha, Turpentine, Interleukin-6, Gene Expression Regulation, Enzymologic, Cytokines, Rats, Sprague-Dawley, Rats, Cyclooxygenase 1, Cyclooxygenase 2

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Effect of acute systemic inflammatory response and cytokines on the transcription of the genes encoding cyclooxygenase enzymes (COX-1 and COX-2) in the rat brain.

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