Cited by 31Pain Mechanisms and TreatmentsGastrointestinal motility and disordersVagus Nerve Stimulation Research

Brain interleukin-1β and tumor necrosis factor-α are involved in lipopolysaccharide-induced delayed rectal allodynia in awake rats

Coelho, Anne-Marie, Fioramonti, Jean, Bueno, Lionel·2000·Brain Research Bulletin

Abstract

Recently, we have developed a model of delayed (12 h) increase in sensitivity (allodynia) to rectal distension (RD) induced by intraperitoneal lipopolysaccharide (LPS) in awake rats. Thus, we examined whether central interleukin-1beta (IL-1beta) and tumor necrosis factor-alpha (TNF-alpha) are involved in LPS response. Abdominal contractions (criterion of visceral pain) were recorded in rats equipped with intramuscular electrodes. RDs were performed at various times after pharmacological treatments. RD induced abdominal contractions from a threshold volume of distension of 0.8 ml. At lowest volume (0.4 ml), this number was significantly increased 12 h after LPS. Intracerebroventricular (i.c.v.) injection of IL-1 receptor antagonist, IL-1beta converting enzyme inhibitor or recombinant human TNF-alpha soluble receptor reduced LPS-induced increase of abdominal contractions at 0.4 ml volume of distension. When injected i.c.v., recombinant human IL-1beta and recombinant bovine TNF-alpha reproduced LPS response at 9 and 12 h and at 6 and 9 h, respectively. These data suggest that IL-1beta and TNF-alpha act centrally to induce delayed rectal hypersensitivity and that central release of these cytokines is responsible of LPS-induced delayed (12 h) rectal allodynia.

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Crossref · 10.1016/s0361-9230(00)00269-0

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  • In animal models, administration of TNFα, IL-1, and IL-6 produces both the illness response and increased sensitivity to noxious stimuli.

    “Administration of inflammatory cytokines TNFa, interleukin-1 (IL-1) and IL-6 in animal models produces both the illness response and increased sensitivity to noxious stimuli”
  • Peripheral lipopolysaccharide in rodents increases pro-inflammatory cytokine expression and causes marked hyperalgesia that is abolished by an IL-1 receptor antagonist or a TNFα antagonist.

    “Lipopolysaccharide administered peripherally in rodents results in enhanced pro-inflammatory cytokine expression and marked hyperalgesia that is abolished by administration of an IL-1 receptor antagonist”

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Authors
Coelho, A.-M., Fioramonti, J., & Bueno, L.
Affiliations
Institut National de Recherche pour l'Agriculture, l'Alimentation et l'Environnement (FR)
Corresponding author
Bueno, Lionel
Venue
Brain Research Bulletin
Publisher
Elsevier BV
Published
2000-06
Volume
52
Issue
3
Pages
223-228
ISSN
0361-9230 (ISSN-L)
OpenAlex
W2070025133
Cited by
31
References
46
Citations by year
2026: 1 · 2022: 1 · 2020: 2 · 2017: 1 · 2016: 1 · 2015: 3 · 2014: 1 · 2013: 2 · 2012: 1
FWCI
1.65
Type
journal article
Language
en
Open access
closed
Locations
  • Brain Research Bulletin (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Physiology › Pain Mechanisms and Treatments
  • Health Sciences › Medicine › Gastroenterology › Gastrointestinal motility and disorders
  • Life Sciences › Neuroscience › Neurology › Vagus Nerve Stimulation Research
Keywords
lipopolysaccharide, IL-1β, TNF-α, visceral pain, rectal distension, central sensitization, intracerebroventricular administration, interleukin-1 receptor antagonist, abdominal contractions, cytokines
MeSH terms
Animals, Brain, Consciousness, Electromyography, Hyperalgesia, Injections, Intraventricular, Interleukin-1, Lipopolysaccharides, Male, Nociceptors, Pain Measurement, Recombinant Proteins, Rectum, Tumor Necrosis Factor-alpha, Viral Proteins, Serpins, Cysteine Proteinase Inhibitors, Rats, Wistar, Rats

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