The cholinergic anti-inflammatory pathway: a missing link in neuroimmunomodulation
Open accessAbstract
This review outlines the mechanisms underlying the interaction between the nervous and immune systems of the host in response to an immune challenge. The main focus is the cholinergic anti-inflammatory pathway, which we recently described as a novel function of the efferent vagus nerve. This pathway plays a critical role in controlling the inflammatory response through interaction with peripheral a7 subunit-containing nicotinic acetylcholine receptors expressed on macrophages. We describe the modulation of systemic and local inflammation by the cholinergic anti-inflammatory pathway and its function as an interface between the brain and the immune system. The clinical implications of this novel mechanism also are discussed.
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The central nervous system can influence peripheral inflammation via efferent vagus nerve activity, which down-regulates inflammation by strongly suppressing TNF gene transcription.
“The central nervous system can also influence peripheral inflammation via efferent vagus nerve activity, which down-regulates inflammation by strongly suppressing TNF gene transcription”
From From stress to inflammation and major depressive disorder: A social signal transduction theory of depression. (2014) · cites this paper as Pavlov, Wang, Czura, Friedman, & Tracey, 2003
The section on parasympathetic control of inflammation reports that efferent vagus stimulation reduces TNF levels, supporting the pathway described. But it says acetylcholine decreases TNF production through a post-transcriptional mechanism, contrary to the claim that the pathway strongly suppresses TNF gene transcription. The indexed passages provide no page number. (LLM, conf=0.90)
Checked by a reasoning model — may be wrong.
Experimental — accuracy not yet measuredThe efferent vagal system can stimulate release of acetylcholine to reduce inflammation and stop the cascading cycle of oxidative damage and inflammation.
“The efferent vagal system can stimulate release of acetylcholine to reduce inflammation and stop the cascading cycle of oxidative damage and inflammation (Pavlov et al., 2003; Namgung et al., 2022).”
From Biobehavioral and psychosocial stress changes during three 8–12 month spaceflight analog missions with Mars-like conditions of isolation and confinement (2022) · cites this paper as Pavlov et al., 2003
In “Evidence for Parasympathetic (Vagus Nerve) Control of Systemic And Local Inflammation” (page unavailable), the paper says acetylcholine suppresses pro-inflammatory cytokines and efferent vagus stimulation reduces TNF in rats. It also says TNF amplifies inflammation partly through reactive oxygen species, but does not establish that vagal signaling stops a cascading cycle of oxidative damage and inflammation. (LLM, conf=0.84)
Experimental — accuracy not yet measuredNo significant differences in either CD3 or I-Ab staining were found between non-implanted and implanted nerve areas as determined by normalised radial distribution analysis extending 150 um from the cross-sectional nerve center.
“No significant differences in either CD3 or l-Ab staining were found between non-implanted and implanted nerve areas (Figure 6) as determined by normalised radial distribution analysis extending 150 um from the cross-sectional nerve center [18].”
From A novel flexible cuff-like microelectrode for dual purpose, acute and chronic electrical interfacing with the mouse cervical vagus nerve (2017) · cites this paper as [18]
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- Authors
- Pavlov, V. A., Wang, H., Czura, C. J., Friedman, S. G., & Tracey, K. J.
- Affiliations
- Northwell Health (US)
- Corresponding author
- Tracey, Kevin J.
- Venue
- Molecular Medicine
- Published
- 2003-05
- Volume
- 9
- Issue
- 5-8
- Pages
- 125-134
- ISSN
- 1076-1551 (ISSN-L)
- 1528-3658
- PMC
- PMC1430829
- OpenAlex
- W1550642465
- Cited by
- 772
- References
- 131
- Citations by year
- 2026: 50 · 2025: 41 · 2024: 47 · 2023: 53 · 2022: 51 · 2021: 43 · 2020: 53 · 2019: 38 · 2018: 33 · 2017: 37 · 2016: 36 · 2015: 32 · 2014: 43 · 2013: 32 · 2012: 33
- FWCI
- 6.55
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Molecular Medicine (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- Defense Advanced Research Projects Agency
- National Institute of General Medical Sciences
- Topics
- Life Sciences › Neuroscience › Neurology › Vagus Nerve Stimulation Research
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuropeptides and Animal Physiology
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Heart Rate Variability and Autonomic Control
- Keywords
- cholinergic anti-inflammatory pathway, neuroimmunomodulation, vagus nerve, macrophages, inflammation, neuroimmune interactions, systemic inflammation, local inflammation
- MeSH terms
- Animals, Antibody Formation, Brain, Humans, Immune System, Inflammation, Vagus Nerve, Neuroimmunomodulation, Cholinergic Agents
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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