The inflammatory reflex
By Kevin J. Tracey. Nature, 2002
3,633 citations recorded by the source corpus.
Subfields: Endocrine and Autonomic Systems, Molecular Biology, Neurology
View Paper: https://www.semanticscholar.org/paper/bf4ad69feceb4719519b726c2337e8fb6b7abe43
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Endocrine and Autonomic Systems
- Bruce S. McEwen
- Peter J. Gianaros
- R. Medzhitov
- Esther M. Sternberg
- Richard C. Becker
- C. Deutschman
- Valentin A. Pavlov
- C. Cunningham
In Molecular Biology
- Kevin J. Tracey
- Bruce S. McEwen
- C. Deutschman
- Peter J. Gianaros
- R. Medzhitov
- Esther M. Sternberg
- Valentin A. Pavlov
- A. Danese
In Neurology
- Kevin J. Tracey
- C. Cunningham
- Bruce S. McEwen
- Peter J. Gianaros
- V. Perry
- C. Deutschman
- R. Medzhitov
- Valentin A. Pavlov
Citations in the corpus
- Neural regulation of innate immunity: a coordinated nonspecific host response to pathogens (2006, background): “This is the first step in the 'inflammatory reflex', which leads to the release of acetylcholine from efferent vagus nerve fibres and resultant negative-feedback control of inflammatio”
- The Cholinergic Anti-inflammatory Pathway: A Missing Link in Neuroimmunomodulation (2003, background): “This previously unrecognized immunomodulatory circuit termed the “cholinergic anti-inflammatory pathway” is a mechanism for neural inhibition of inflammation (18,19), and interfaces the brain with the immune system.”
- The role of inflammation in epilepsy (2010, neutral): “50”
- Cytokines and major depression. (2005, background): “studied by Yirmiya (1996). The effects of the bacterial endotoxin LPS, which is a potent activator of the immune system, on affective and cognitive functions were investigated in healthy human volunteers.”
- Splenic nerve is required for cholinergic antiinflammatory pathway control of TNF in endotoxemia (2008, background): “However, this observation does not take into account the requirement of nicotinic acetylcholine receptor 7 subunit signaling in the cholinergic antiinflammatory pathway (3, 28).”
- Adverse childhood experiences, allostasis, allostatic load, and age-related disease. (2012, background): “The elevation in inflammation levels is presumably due to the chronic or repeated stimulation of the sympathetic nervous system [15], as well as to the progressive down-regulation of key anti-inflammatory pathways, such as the HPA axis [24,28] and the parasympathetic nervous system [29,30].”
- Systemic infections and inflammation affect chronic neurodegeneration (2007, background): “First, inflammatory events in the thoracic abdominal cavity are signalled to the brain through vagal-nerve sensory afferents, and in turn the vagal efferent outflow might modify these inflammatory events through acetylcholine secretio”
- Immune modulation of learning, memory, neural plasticity and neurogenesis. (2011, neutral): “Since both in the periphery and the brain ACh produces anti-inflammatory effects (Pollak et al., 2005; Tracey, 2002), elevation of AChE activity can produce further cytokine secretion and such effects were suggested to be involved in stress- and endotoxin-induced memory disturbances in humans…”
- The alpha7 nicotinic acetylcholine receptor as a pharmacological target for inflammation (2007, background): “Nicotine exerts anti-inflammatory effects on macrophages that can be counteracted by selective a7-antagonists (Tracey, 2002; Wang et al., 2003; Ulloa, 2005).”
- Anxiety Disorders are Associated with Reduced Heart Rate Variability: A Meta-Analysis (2014, background): “This chronicity may in turn contribute to chronic withdrawal of the parasympathetic nervous system, and subsequent impairment in the cholinergic anti-inflammatory reflex (107), leading to an increase in a host of conditions including diabetes, obesity, and CVD (9, 10).”
- Physiology and immunology of the cholinergic antiinflammatory pathway. (2007, positive): “Accord-ingly, it seemed possible to posit the existence of a comparable mechanism to control cytokine release that could, at least in theory, function as an extremely fast, reflex-like antiinflammatory pathway controlled by brain networks (14).”
- Sepsis: current dogma and new perspectives. (2014, background): “The inflammatory reflex is a prototypical, major efferent neural pathway that modulates TNF release in response to LPS (Figure 2) (Tracey, 2002, 2009; Borovikova et al., 2000).”