ArticleJournal of internal medicine2024
Circulating extracellular choline acetyltransferase regulates inflammation.
Article in Journal of internal medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 9 citations in OpenAlex.
- Dynamic Changes in Serum Choline Acetyltransferase and Acetylcholinesterase in Septic versus Non-Septic ICU Patients: A Prospective Exploratory Study.Journal of inflammation research · 2026Trial
- Sodium bicarbonate attenuates myocardial ischemia-reperfusion injury via activation of the splenic cholinergic anti-inflammatory pathway.JTCVS open · 2026Article
- Neuroimmune related pathway may involve in neuropathic pain after brachial plexus injury: a clinical and experimental discovery.Open life sciences · 2026Article
- A new combined prognostic model involvingTranslational cancer research · 2025Article
- Nociceptor α7nAChR activation blunts neuronal HMGB1 release and attenuates inflammation and nociceptive behavior.Molecular medicine (Cambridge, Mass.) · 2025Article
- Choline in immunity: a key regulator of immune cell activation and function.Frontiers in immunology · 2025Review
- Article
- Cholinergic macrophages promote the resolution of peritoneal inflammation.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Dysregulated brain-gut axis in the setting of traumatic brain injury: review of mechanisms and anti-inflammatory pharmacotherapies.Journal of neuroinflammation · 2024Review
- Contributions of Non-Neuronal Cholinergic Systems to the Regulation of Immune Cell Function, Highlighting the Role of α7 Nicotinic Acetylcholine Receptors.International journal of molecular sciences · 2024Review
Corrections and comments
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Authors and funding
15 authors at 1 institution in 1 country.
Funding
Abstract
backgroundCholine acetyltransferase (ChAT) is required for the biosynthesis of acetylcholine, the molecular mediator that inhibits cytokine production in the cholinergic anti-inflammatory pathway of the vagus nerve inflammatory reflex. Abundant work has established the biology of cytoplasmic ChAT in neurons, but much less is known about the potential presence and function of ChAT in the extracellular milieu.
objectivesWe evaluated the hypothesis that extracellular ChAT activity responds to inflammation and serves to inhibit cytokine release and attenuate inflammation.
methodsAfter developing novel methods for quantification of ChAT activity in plasma, we determined whether ChAT activity changes in response to inflammatory challenges.
resultsActive ChAT circulates within the plasma compartment of mice and responds to immunological perturbations. Following the administration of bacterial endotoxin, plasma ChAT activity increases for 12-48 h, a time period that coincides with declining tumor necrosis factor (TNF) levels. Further, a direct activation of the cholinergic anti-inflammatory pathway by vagus nerve stimulation significantly increases plasma ChAT activity, whereas the administration of bioactive recombinant ChAT (r-ChAT) inhibits endotoxin-stimulated TNF production and anti-ChAT antibodies exacerbate endotoxin-induced TNF levels, results of which suggest that ChAT activity regulates endogenous TNF production. Administration of r-ChAT significantly attenuates pro-inflammatory cytokine production and disease activity in the dextran sodium sulfate preclinical model of inflammatory bowel disease. Finally, plasma ChAT levels are also elevated in humans with sepsis, with the highest levels observed in a patient who succumbed to infection.
conclusionAs a group, these results support further investigation of ChAT as a counter-regulator of inflammation and potential therapeutic agent.
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