Immune system to brain signaling: Neuropsychopharmacological implications
Open accessAbstract
There has been an explosion in our knowledge of the pathways and mechanisms by which the immune system can influence the brain and behavior. In the context of inflammation, pro-inflammatory cytokines can access the central nervous system and interact with a cytokine network in the brain to influence virtually every aspect of brain function relevant to behavior including neurotransmitter metabolism, neuroendocrine function, synaptic plasticity, and neurocircuits that regulate mood, motor activity, motivation, anxiety and alarm. Behavioral consequences of these effects of the immune system on the brain include depression, anxiety, fatigue, psychomotor slowing, anorexia, cognitive dysfunction and sleep impairment; symptoms that overlap with those which characterize neuropsychiatric disorders, especially depression. Pathways that appear to be especially important in immune system effects on the brain include the cytokine signaling molecules, p38 mitogen-activated protein kinase and nuclear factor kappa B; indoleamine 2,3 dioxygenase and its downstream metabolites, kynurenine, quinolinic acid and kynurenic acid; the neurotransmitters, serotonin, dopamine and glutamate; and neurocircuits involving the basal ganglia and anterior cingulate cortex. A series of vulnerability factors including aging and obesity as well as chronic stress also appears to interact with immune to brain signaling to exacerbate immunologic contributions to neuropsychiatric disease. The elucidation of the mechanisms by which the immune system influences behavior yields a host of targets for potential therapeutic development as well as informing strategies for the prevention of neuropsychiatric disease in at risk populations.
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Individuals with a history of depression are more likely to develop cognitive and affective symptoms of depression following IFNα treatment for cancer or hepatitis C than persons without a history of depression.
“individuals with a history of depression are more likely to develop cognitive and affective symptoms of depression (e.g., depressed mood, anxiety, irritability, memory and attentional problems) following IFNα treatment for cancer or hepatitis C than persons without a history of depression”
From From stress to inflammation and major depressive disorder: A social signal transduction theory of depression. (2014) · cites this paper as Capuron & Miller, 2011
The section on cytokine-induced neuropsychiatric symptoms (page unavailable) says that mood and cognitive symptoms can follow IFN-alpha treatment for cancer or hepatitis C, especially in patients with vulnerability factors. It identifies preexisting subclinical depressive traits as a risk factor, but does not specifically compare people with and without a history of depression. (LLM, conf=0.85)
Experimental — accuracy not yet measuredNearly all patients who receive IFNα treatment for these conditions appear to experience a sudden onset of neurovegetative symptoms of depression, including anorexia, fatigue, psychomotor retardation, and disrupted sleep.
“nearly all patients who receive IFNα treatment for these conditions appear to experience a sudden onset of neurovegetative symptoms of depression, including anorexia, fatigue, psychomotor retardation, and disrupted sleep”
From From stress to inflammation and major depressive disorder: A social signal transduction theory of depression. (2014) · cites this paper as Capuron & Miller, 2011
Together, this pathway may cause cellular damage and volume loss in the hippocampus and medial prefrontal cortex.
“Together, this pathway may trigger hippocampal and mPFC cellular damage and volume reductions (138,144,145).”
From The Impact of Stress and Major Depressive Disorder on Hippocampal and Medial Prefrontal Cortex Morphology (2019) · cites this paper as [144]
Peripherally produced cytokines can influence the central nervous system.
“peripherally produced cytokines can influence the central nervous system (CNS)”
From Cytokine Research in Depression: Principles, Challenges, and Open Questions (2019) · cites this paper as [31]
Most studies measure serum or plasma cytokine levels, but it has often been discussed whether these results reflect the situation in the brain.
“Most of the studies measure serum or plasma cytokine levels, but it has often been discussed whether these results reflect the situation in the brain (31).”
From Cytokine Research in Depression: Principles, Challenges, and Open Questions (2019) · cites this paper as [31]
Cytokines have been shown to be altered in other psychiatric disorders.
“they have also been shown to be altered in other psychiatric disorders.”
From Cytokine Research in Depression: Principles, Challenges, and Open Questions (2019) · cites this paper as [31]
Elevated levels of tumor necrosis factor-alpha have also been found in PTSD studies, in patients with anorexia nervosa and in patients with acute relapse of schizophrenia.
“For example, elevated levels of TNF-α have also been found in PTSD studies (34), in patients with anorexia nervosa (37) and in patients with acute relapse of schizophrenia (31, 38).”
From Cytokine Research in Depression: Principles, Challenges, and Open Questions (2019) · cites this paper as [31]
Pro-inflammatory cytokines can enter the brain and lead to changes in neurotransmitter systems involved in the development of depression, such as the serotonin system.
“and these cytokines could then enter the brain (31) and lead to changes in neurotransmitter systems involved in the development of depression, such as the serotonin system (82, 83, 85, 86, 182).”
From Cytokine Research in Depression: Principles, Challenges, and Open Questions (2019) · cites this paper as [31]
Peripheral inflammatory processes are capable of inducing neuroinflammatory processes through several well-characterized immune-to-brain signaling pathways.
“peripheral inflammatory processes are capable of inducing neuroinflammatory processes through several well-characterized immune-to-brain signaling pathways (for a review see Capuron and Miller, 2011)”
From Danger Signals and Inflammasomes: Stress-Evoked Sterile Inflammation in Mood Disorders (2017) · cites this paper as Capuron and Miller, 2011
Multiple non-exclusive pathways activate the HPA axis upon cerebral or peripheral immune challenges, including local inflammatory mediators, circulating factors accessing the PVN via circumventricular organs or a disrupted blood-brain barrier, endothelial signaling, and vagus nerve afferents.
“Multiple non-exclusive pathways participate in the activation of the HPA axis upon cerebral or peripheral immune challenges. When an immunogenic insult takes place in the brain, various inflammatory mediators produced locally may trigger the HPA axis.”
From The HPA – Immune Axis and the Immunomodulatory Actions of Glucocorticoids in the Brain (2014) · cites this paper as [14]
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- Authors
- Capuron, L., & Miller, A. H.
- Affiliations
- Emory University (US)
- Corresponding author
- Capuron, Lucile
- Miller, Andrew H.
- Venue
- Pharmacology & Therapeutics
- Publisher
- Elsevier BV
- Published
- 2011-05
- Volume
- 130
- Issue
- 2
- Pages
- 226-238
- ISSN
- 0163-7258 (ISSN-L)
- PMC
- PMC3072299
- OpenAlex
- W2072016770
- Cited by
- 1,195
- References
- 199
- Citations by year
- 2026: 74 · 2025: 91 · 2024: 74 · 2023: 68 · 2022: 75 · 2021: 102 · 2020: 97 · 2019: 77 · 2018: 88 · 2017: 59 · 2016: 76 · 2015: 81 · 2014: 69 · 2013: 80 · 2012: 61
- FWCI
- 3.76
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Pharmacology & Therapeutics (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- HAL (submittedVersion)
- Funders
- National Institute of Mental Health (R01MH083746, R01MH087604, R01MH075102)
- 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
- neuroinflammation, inflammatory cytokines, depression, anxiety, p38 MAPK, NF-κB, indoleamine 2,3-dioxygenase, kynurenine pathway, serotonin, dopamine, glutamate, basal ganglia, anterior cingulate cortex, chronic stress, aging, obesity, neuropsychiatric disorders, therapeutic target
- MeSH terms
- Animals, Mental Disorders, Brain, Humans, Inflammation, Models, Neurological, Neuroimmunomodulation, Cytokines, Drug Delivery Systems, Inflammation Mediators, Translational Research, Biomedical
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