Cited by 789Tryptophan and brain disordersNeuroinflammation and Neurodegeneration MechanismsStress Responses and Cortisol

Cytokine, Sickness Behavior, and Depression

Open access
Dantzer, Robert·2009·Immunology and Allergy Clinics of North America

Abstract

The psychologic and behavioral components of sickness represent, together with fever response and associated neuroendocrine changes, a highly organized strategy of the organism to fight infection. This strategy, referred to as sickness behavior, is triggered by the proinflammatory cytokines produced by activated cells of the innate immune system in contact with specific pathogen-associated molecular patterns (PAMPs). Interleukin-1 and other cytokines act on the brain via (1) a neural route represented by the primary afferent neurons that innervate the body site where the infectious process takes place and (2) a humoral pathway that involves the production of proinflammatory cytokines. This article presents the current knowledge on the way this communication system is organized and regulated and the implications of these advances for understanding brain physiology and pathology.

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Crossref · 10.1016/j.iac.2009.02.002

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  • Clinical studies report higher levels of circulating pro-inflammatory cytokines in MDD patients, a pattern replicated in preclinical animal models of depression.

    “clinical studies report higher levels of circulating pro-inflammatory cytokines in MDD patients, a pattern that has been replicated in preclinical animal models of depression1, 7–10.”

    From Social stress induces neurovascular pathology promoting depression (2017) · cites this paper as [9]

    The Pathophysiologic implications section reports elevated circulating proinflammatory cytokines, particularly IL-6, in major depression. It also describes depressive-like behavior in mice subjected to inflammation, but does not say that elevated circulating cytokine levels in depressed patients were replicated in animal models. Page numbers were not available in our copy. (LLM, conf=0.86)

    Experimental — accuracy not yet measured
  • Heightened peripheral inflammation contributes to the pathogenesis of major depressive disorder.

    “Studies suggest that heightened peripheral inflammation contributes to the pathogenesis of major depressive disorder.”

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Authors
Dantzer, R.
Affiliations
University of Illinois Urbana-Champaign (US)
Corresponding author
Dantzer, Robert
Venue
Immunology and Allergy Clinics of North America
Publisher
Elsevier BV
Published
2009-05
Volume
29
Issue
2
Pages
247-264
ISSN
0889-8561 (ISSN-L)
OpenAlex
W2031045752
Cited by
789
References
12
Citations by year
2026: 25 · 2025: 26 · 2024: 54 · 2023: 71 · 2022: 67 · 2021: 76 · 2020: 80 · 2019: 52 · 2018: 64 · 2017: 39 · 2016: 38 · 2015: 40 · 2014: 37 · 2013: 32 · 2012: 36
FWCI
9.27
Type
journal article
Language
en
Open access
Locations
  • Immunology and Allergy Clinics of North America (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
National Institute of Mental Health (R01MH079829, R01MH071349)
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, inflammatory cytokines, depression, interleukin-1, innate immune system, pathogen-associated molecular patterns, fever response, neuroendocrine changes, primary afferent neurons, brain-immune communication, infection

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