Abstract

Sickness behavior refers to the coordinated set of behavioral changes that develop in sick individuals during the course of an infection. At the molecular level, these changes are due to the effects of proinflammatory cytokines, such as interleukin-1 (IL-1) and tumor necrosis factor-alpha (TNFalpha), in the brain. Peripherally released cytokines act on the brain via a fast transmission pathway involving primary afferent nerves innervating the body site of inflammation and a slow transmission pathway involving cytokines originating from the choroid plexus and circumventricular organs and diffusing into the brain parenchyma by volume transmission. At the behavioral level, sickness behavior appears to be the expression of a central motivational state that reorganizes the organism's priorities to cope with infectious pathogens. There is clinical and experimental evidence that activation of the brain cytokine system is associated with depression, although the exact relationship between sickness behavior and depression is still elusive.

Keywords

Sickness behaviorCircumventricular organsProinflammatory cytokineChoroid plexusCytokineTumor necrosis factor alphaImmunologyInflammationNeuroscienceMedicineCentral nervous systemPsychology

MeSH Terms

BrainCytokinesHumansNeuroimmunomodulationPsychoneuroimmunologySick Role

Affiliated Institutions

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Publication Info

Year
2001
Type
review
Volume
15
Issue
1
Pages
7-24
Citations
845
Access
Closed

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Citation Metrics

845
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48
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663
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Cite This

Robert Dantzer (2001). Cytokine-Induced Sickness Behavior: Where Do We Stand?. Brain Behavior and Immunity , 15 (1) , 7-24. https://doi.org/10.1006/brbi.2000.0613

Identifiers

DOI
10.1006/brbi.2000.0613
PMID
11259077

Data Quality

Data completeness: 86%