Cited by 135Inflammatory mediators and NSAID effectsTryptophan and brain disordersNeuroinflammation and Neurodegeneration Mechanisms

Prostaglandins and sickness behavior: Old story, new insights

Pecchi, Emilie, Dallaporta, Michel, Jean, André, Thirion, Sylvie, Troadec, Jean-Denis·2009·Physiology & Behavior

Abstract

Previous evidence has shown that prostaglandins play a key role in the development of sickness behavior observed during inflammatory states. In particular, prostaglandin E2 (PGE2) is produced in the brain by a variety of inflammatory signals such as endotoxins or cytokines. Its injection has been also shown to induce symptoms of sickness behavior. The role of cyclooxygenase enzymes (COX), the rate-limiting enzymes converting arachidonic acid into prostaglandins, in sickness behavior has been extensively studied, and it has been demonstrated that strategies aiming at inhibiting these enzymes limit anorexia, body weight loss and fever in animals with inflammatory diseases. However, inhibiting COX activity may lead to negative gastric or cardiovascular effects, since COX enzymes play a role in the synthesis of others prostanoids with various and sometimes contrasting properties. Recently, prostaglandin E synthases (PGES), which specifically catalyze the final step of PGE2 biosynthesis, were characterized. Among these enzymes, the microsomal prostaglandin E synthase-1 (mPGES-1) was of a particular interest since it was shown to be up-regulated by inflammatory signals in a variety of cell types. Moreover, mPGES-1 was shown to be crucial for correct immune-to-brain communication and induction of fever and anorexia by pro-inflammatory agents. This review takes stock of previous knowledge and recent advances in understanding the role of prostaglandins and of their specific synthesizi…

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Crossref · 10.1016/j.physbeh.2009.02.040

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  • Inflammatory challenges involving administration of proinflammatory cytokines ILβ or TNFα trigger a constellation of sickness behaviors in rodents including hypersomnia, fatigue, anorexia, impaired cognitive abilities, psychomotor retardation, and reduced social and exploratory behavior.

    “inflammatory challenges that involve administration of the proinflammatory cytokines ILβ or TNFα trigger a constellation of several sickness behaviors in rodents that includes hypersomnia, fatigue, anorexia, impaired cognitive abilities, psychomotor retardation, and reduced social and exploratory behavior”

    From From stress to inflammation and major depressive disorder: A social signal transduction theory of depression. (2014) · cites this paper as Pecchi, Dallaporta, Jean, Thirion, & Troadec, 2009

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Authors
Pecchi, E., Dallaporta, M., Jean, A., Thirion, S., & Troadec, J.-D.
Affiliations
Centre National de la Recherche Scientifique (FR)
Corresponding author
Troadec, Jean-Denis
Venue
Physiology & Behavior
Publisher
Elsevier BV
Published
2009-06
Volume
97
Issue
3-4
Pages
279-292
ISSN
0031-9384 (ISSN-L)
OpenAlex
W2068294577
Cited by
135
References
12
Citations by year
2026: 2 · 2025: 6 · 2024: 3 · 2023: 2 · 2022: 9 · 2021: 9 · 2020: 6 · 2019: 9 · 2018: 11 · 2017: 4 · 2016: 11 · 2015: 10 · 2014: 8 · 2013: 8 · 2012: 11
FWCI
1.30
Type
journal article
Language
en
Open access
closed
Locations
  • Physiology & Behavior (publishedVersion)
  • PubMed (publishedVersion)
  • HAL (submittedVersion)
Funders
  • Centre National de la Recherche Scientifique
  • Institut National de la Recherche Agronomique
Topics
  • Health Sciences › Medicine › Pharmacology › Inflammatory mediators and NSAID effects
  • Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords
prostaglandins, sickness behavior, prostaglandin E2, cyclooxygenase, prostaglandin E synthase, mPGES-1, inflammation, fever, anorexia, arachidonic acid metabolism, cyclooxygenase inhibitors, prostanoids
MeSH terms
Animals, Brain, Humans, Prostaglandin-Endoperoxide Synthases, Prostaglandins, Illness Behavior

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