Cited by 249Tryptophan and brain disordersNeuroinflammation and Neurodegeneration MechanismsStress Responses and Cortisol

Molecular Basis of Sickness Behaviora

DANTZER, ROBERT, BLUTHÉ, ROSE‐MARIE, GHEUSI, GILLES, CREMONA, SANDRINE, LAYÉ, SOPHIE, PARNET, PATRICIA, KELLEY, KEITH W.·1998·Annals of the New York Academy of Sciences

Abstract

ABSTRACT: Peripheral and central injections of lipopolysaccharide (LPS), a cytokine inducer, and recombinant proinflammatory cytokines such as interleukin‐1β (IL‐1β) induce sickness behavior in the form of reduced food intake and decreased social activities. Mechanisms of the behavioral effects of cytokines have been the subject of much investigation during the last 3 years. At the behavioral level, the profound depressing effects of cytokines on behavior are the expression of a highly organized motivational state. At the molecular level, sickness behavior is mediated by an inducible brain cytokine compartment that is activated by peripheral cytokines via neural afferent pathways. Centrally produced cytokines act on brain cytokine receptors that are similar to those characterized on peripheral immune and nonimmune cells, as demonstrated by pharmacologic experiments using cytokine receptor antagonists, neutralizing antibodies to specific subtypes of cytokine receptors, and gene targeting techniques. Evidence exists that different components of sickness behavior are mediated by different cytokines and that the relative importance of these cytokines is not the same in the peripheral and central cytokine compartments.

Integrity signals

Registry

Crossref · 10.1111/j.1749-6632.1998.tb08321.x

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  • Activation of proinflammatory signaling molecules engages neural mechanisms that mediate changes to mood, cognition, and physiology that are adaptive for host defense against infection or injury (sickness response).

    “This argument comes from the observation that activation of proinflammatory signaling molecules engage neural mechanisms that mediate changes to mood, cognition, and physiology that are adaptive for the host defense against infection or injury (ie, the 'sickness' response) (Dantzer et al, 1998;Maier and Watkins, 1998).”

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Authors
DANTZER, R., BLUTHÉ, R., GHEUSI, G., CREMONA, S., LAYÉ, S., PARNET, P., & KELLEY, K. W.
Affiliations
  • Inserm (FR)
  • University of Illinois Urbana-Champaign (US)
Corresponding author
DANTZER, ROBERT
Venue
Annals of the New York Academy of Sciences
Publisher
Wiley
Published
1998-09
Volume
856
Issue
1
Pages
132-138
ISSN
  • 0077-8923 (ISSN-L)
  • 1749-6632
OpenAlex
W1992350503
Cited by
249
References
23
Citations by year
2026: 3 · 2025: 5 · 2024: 3 · 2023: 6 · 2022: 5 · 2021: 6 · 2020: 2 · 2019: 7 · 2018: 3 · 2017: 3 · 2016: 8 · 2015: 11 · 2014: 10 · 2013: 10 · 2012: 12
FWCI
3.87
Type
journal article
Language
en
Open access
closed
Locations
  • Annals of the New York Academy of Sciences (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (5r01dk049311-05)
  • National Institute of Mental Health (R01MH051569, MH51569)
  • National Institute of Diabetes and Digestive and Kidney Diseases (DK 49311)
Topics
  • Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
Keywords
sickness behavior, lipopolysaccharide, IL-1β, inflammatory cytokines, cytokine receptor antagonists, dietary intake, social behavior, gene targeting
MeSH terms
Animals, Behavior, Animal, Brain, Disease, Feeding Behavior, Humans, Inflammation, Lipopolysaccharides, Recombinant Proteins, Social Behavior, Cytokines

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