The cholinergic anti-inflammatory pathway.
By Valentin A. Pavlov, Kevin J. Tracey. Brain, behavior, and immunity, 2005
599 citations recorded by the source corpus.
Subfields: Molecular Biology, Neurology, Sensory Systems
View Paper: https://www.semanticscholar.org/paper/4331367cce6a9560d5a781c158bdb4b1dcf4e999
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Molecular Biology
- M. Fuller
- Rachel I. Wilson
- C. Kirkpatrick
- Kristin Scott
- Gregory S. X. E. Jefferis
- Liqun Luo
- S. Waddell
- Jure Leskovec
In Neurology
- C. Kirkpatrick
- S. Waddell
- Gregory E. Miller
- Emeran A. Mayer
- Charles L Raison
- I. Wessler
- L. Capuron
- Andrew H. Miller
In Sensory Systems
- Liqun Luo
- Gregory S. X. E. Jefferis
- Rachel I. Wilson
- Kristin Scott
- S. Waddell
- Emeran A. Mayer
- Glenn C. Turner
- Gilles Laurent
Citations in the corpus
- Fly Cell Atlas: a single-nucleus transcriptomic atlas of the adult fruit fly (2022, background): “Finally, expression of acetylcholine receptors was specific for a subset of hemocytes, relating to the cholinergic anti-inflammatory pathway as described in humans and mice (26).”
- Inflammation and Its Discontents: The Role of Cytokines in the Pathophysiology of Major Depression (2009, unknown): “In addition, in vitro studies have demonstrated that stimulation of both alpha- and beta-adrenergic receptors can activate inflammatory signaling pathways, including NF-κB(87).”
- Cytokines sing the blues: inflammation and the pathogenesis of depression. (2006, background): “Vagal withdrawal in response to stress might also promote inflammation, given the evidence that vagal activity inhibits NFkB activation (and the release of TNF-α from macrophages) via cholinergic signaling through the α-7 subunit of the nicotinic acetylcholine receptor [77].”
- Inflammatory processes in Alzheimer's disease. (2007, unknown): “Thus, neurons can serve as source of complement, COX-2-derived prostanoids (Davis and Laroche, 2003; Pavlov and Tracey, 2005; Rozemuller et al., 1989b; Simard et al., 2006; Natarajan and Bright, 2002; Moore et al., 2005), and several cytokines including IL-1β, IL-6, and TNF-α (Botchkina et al.,…”
- Psychological Stress in Childhood and Susceptibility to the Chronic Diseases of Aging: Moving Towards a Model of Behavioral and Biological Mechanisms (2011, background): “Haensel et al. (2008); Marsland et al. (2007); Pavlov and Tracey (2005) - Oxytocin concentrations are lower in individuals who have experienced maltreatment relative to controls.”
- Acetylcholine beyond neurons: the non‐neuronal cholinergic system in humans (2008, background): “Macrophages, mononuclear cells a7 Anti-inflammatory effects, release of proinflammatory cytokines k Shytle et al. (2004); Pavlov and Tracey (2005) T cells a7 Interaction with TRC, Cain m Razani-Boroujerdi et al. (2007) B cells a7 Regulation of antibody production Kawashima et al. (2007) Mucosal…”
- The effects of acute psychological stress on circulating and stimulated inflammatory markers: A systematic review and meta-analysis (2017, background): “The PNS acts through acetylcholine receptors in immune cells to down-regulate pro-inflammatory cytokine production (Borovikova et al., 2000; Marsland, Gianaros, Prather, Manuck, 2007) and circulating markers of inflammation (Sloan et al., 2007; Pavlov & Tracey, 2005).”
- Cytokines and their relationship to the symptoms and outcome of cancer (2008, background): “Although often overlooked, neuronal pathways and hormones (such as cortisol and adrenaline”
- Gut feelings: the emerging biology of gut–brain communication (2011, background): “Vagal modulation of macrophage activation through nicotinic acetylcholine receptors has been reported as part of a vago–vagal anti-inflammatory refle”
- The Effect of Antidepressant Medication Treatment on Serum Levels of Inflammatory Cytokines: A Meta-Analysis (2011, unknown): “An elevated level of circulating inflammatory cytokines may occur because of a dysfunction in the brain’s anti-inflammatory mechanisms, which include the hypothalamic–pituitary–adrenal axis, the efferent vagus (Bierhaus et al, 2003; Pavlov and Tracey, 2005; Shaked et al, 2009), and noradrenergic inn”