The Cholinergic Anti-Inflammatory Pathway: A Novel Paradigm for Translational Research in Neuroimmunology

Cuoco, Joshua A.; Fennie, Charles N

doi:10.21767/2171-6625.100086

Cited by 12 publications

(12 citation statements)

References 35 publications

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“…97 Activation of α7nAChR stimulates the janus kinase 2 (JAK2)/signal transducers and activators of transcription 3 (STAT3) signalling pathway which inhibits transcriptional activity of NF-κB, resulting in reduced pro-inflammatory cytokine production. [98][99][100] In addition, α7nAChR activation inhibits phosphorylation of an inhibitor of kappa B (IκB), which inhibits nuclear translocation of NF-κB independent of the JAK2/STAT3 pathway. 99 Recently, Li et al reported that α7nAChR activation decreased glycogen synthase kinase-3β (GSK-3β) activity through phosphorylation at Serine 9 and reduced NF-κB activation, thus inhibiting proinflammatory cytokine production.…”

Section: Models Of Hfmentioning

confidence: 99%

“…[98][99][100] In addition, α7nAChR activation inhibits phosphorylation of an inhibitor of kappa B (IκB), which inhibits nuclear translocation of NF-κB independent of the JAK2/STAT3 pathway. 99 Recently, Li et al reported that α7nAChR activation decreased glycogen synthase kinase-3β (GSK-3β) activity through phosphorylation at Serine 9 and reduced NF-κB activation, thus inhibiting proinflammatory cytokine production. 101 Furthermore, m 2 AChR activation reduced the level of proinflammatory cytokines through regulation of MAPKs phosphorylation (ie p38 MAPK and c-Jun N-terminal kinase [JNK]).…”

Section: Models Of Hfmentioning

confidence: 99%

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The effects of acetylcholinesterase inhibitors on the heart in acute myocardial infarction and heart failure: From cells to patient reports

2019

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Cardiovascular diseases remain a major cause of morbidity and mortality worldwide. Cardiovascular diseases such as acute myocardial infarction, ischaemia/reperfusion injury and heart failure are associated with cardiac autonomic imbalance characterized by sympathetic overactivity and parasympathetic withdrawal from the heart. Increased parasympathetic activity by electrical vagal nerve stimulation has been shown to provide beneficial effects in the case of cardiovascular diseases in both animals and patients by improving autonomic function, cardiac remodelling and mitochondrial function. However, clinical limitations for electrical vagal nerve stimulation exist because of its invasive nature, costly equipment and limited clinical validation. Therefore, novel therapeutic approaches which moderate parasympathetic activities could be beneficial for in the case of cardiovascular disease. Acetylcholinesterase inhibitors inhibit acetylcholinesterase and hence increase cholinergic transmission. Recent studies have reported that acetylcholinesterase inhibitors improve autonomic function and cardiac function in cardiovascular disease models. Despite its potential clinical benefits for cardiovascular disease patients, the role of acetylcholinesterase inhibitors in acute myocardial infarction and heart failure remediation remains unclear. This article comprehensively reviews the effects of acetylcholinesterase inhibitors on the heart in acute myocardial infarction and heart failure scenarios from in vitro and in vivo studies to clinical reports. The mechanisms involved are also discussed in this review.

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Section: Models Of Hfmentioning

confidence: 99%

Section: Models Of Hfmentioning

confidence: 99%

The effects of acetylcholinesterase inhibitors on the heart in acute myocardial infarction and heart failure: From cells to patient reports

2019

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“…These signals are converted to the nucleus tractus solitarius and project to autonomic output centers (eg, limbic system, hippocampus, frontal cortex). The medulla coordinates this response and stimulates vagal efferent fibers, which project to the celiac ganglion 26. Vagal fibers develop synapses on cell bodies within the celiac ganglion, thus activating innate immune responses in the spleen.…”

Section: The Vagus Nerve’s Inflammatory Association With Hiv and Deprmentioning

confidence: 99%

The potential role of vagus-nerve stimulation in the treatment of HIV-associated depression: a review of literature

Nicholson¹,

Kempf²,

Moneyham³

et al. 2017

NDT

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Depression is the most common comorbidity and neuropsychiatric complication in HIV. Estimates suggest that the prevalence rate for depression among HIV-infected individuals is three times that of the general population. The association between HIV and clinical depression is complex; however, chronic activation of inflammatory mechanisms, which disrupt central nervous system (CNS) function, may contribute to this association. Disruptions in CNS function can result in cognitive disorders, social withdrawal, fatigue, apathy, psychomotor impairment, and sleep disturbances, which are common manifestations in depression and HIV alike. Interestingly, the parasympathetic system-associated vagus nerve (VN) has primary homeostatic properties that restore CNS function following a stress or inflammatory response. Unfortunately, about 30% of adults with HIV are resistant to standard psychotherapeutic and psychopharmacological treatments for depression, thus suggesting the need for alternative treatment approaches. VN stimulation (VNS) and its benefits as a treatment for depression have been well documented, but remain unexplored in the HIV population. Historically, VNS has been delivered using a surgically implanted device; however, transcutanous VNS (tVNS) with nonsurgical auricular technology is now available. Although it currently lacks Food and Drug Administration approval in the US, evidence suggests several advantages of tVNS, including a reduced side-effect profile when compared to standard treatments and comparable results to implantable VNS in treating depression. Therefore, tVNS could offer an alternative for managing depression in HIV via regulating CNS function; moreover, tVNS may be useful for treatment of other symptoms common in HIV. From this, implications for nursing research and practice are provided.

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“…Emerging evidence has begun to depict the molecular mechanisms by which inflammation is regulated via the nervous system [6][7][8][9][10][11][12][13][14][15][16][17][18]. Specifically, inflammation is controlled by neuroimmunologic circuitry, dependent on the vagus nerve, operating in a reflexive continuum.…”

Section: Introductionmentioning

confidence: 99%

“…The vagus nerve activates the cholinergic anti-inflammatory pathway via projection to the celiac ganglion, not the heart [6][7][8][9][10][11][12][13][14][15][16][17][18]. Although it would be ideal for previous OMT studies to indicate an association between suboccipital decompression and stimulation of vagal efferents projecting to the celiac ganglion, there are currently no such studies that demonstrate this relationship in the osteopathic literature.…”

Section: Introductionmentioning

confidence: 99%

Hypothetical Link Between Osteopathic Suboccipital Decompression and Neuroimmunomodulation

Cuoco

Fennie²,

Cheriyan³

2016

J Neurol Neurosci

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Emerging evidence has begun to depict the molecular mechanisms by which inflammation is regulated via the vagus nerve. Specifically, inflammation can be controlled by neuroimmunologic circuitry, dependent upon vagal afferent and efferent fibers, operating in a reflexive continuum. This neuro-immune reflex, known as the inflammatory reflex arc, has some control on serum concentrations of numerous molecular mediators of inflammation such as C-reactive protein and interleukin-6. Importantly, both of these inflammatory proteins are elevated in acute ST-elevation myocardial infarction and are associated with worse cardiac sequelae. Suboccipital decompression by osteopathic manual treatment has been demonstrated to enhance vagal output to the heart, as measured by increased high frequency spectral power of heart rate variability, in a statistically significant manner further supported by a significant decrease in the low-/high frequency spectral power ratio among healthy adults compared to sham treatment and time control. Considering this association, we postulate that suboccipital decompression may stimulate the efferent branch of this vagal-mediated reflex, the cholinergic antiinflammatory pathway, thereby suppressing C-reactive protein and interleukin-6 levels post-ST-elevation myocardial infarction. Furthermore, we provide a detailed clinical study that can determine the validity of our hypothesis.

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The Cholinergic Anti-Inflammatory Pathway: A Novel Paradigm for Translational Research in Neuroimmunology

Cited by 12 publications

References 35 publications

The effects of acetylcholinesterase inhibitors on the heart in acute myocardial infarction and heart failure: From cells to patient reports

The effects of acetylcholinesterase inhibitors on the heart in acute myocardial infarction and heart failure: From cells to patient reports

The potential role of vagus-nerve stimulation in the treatment of HIV-associated depression: a review of literature

Hypothetical Link Between Osteopathic Suboccipital Decompression and Neuroimmunomodulation

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