Immunologic Role of the Cholinergic Anti-Inflammatory Pathway and the Nicotinic Acetylcholine  7 Receptor

2005 ◽  
Vol 1062 (1) ◽  
pp. 209-219 ◽  
Author(s):  
M. GALLOWITSCH-PUERTA
Keyword(s):  
Nicotinic Acetylcholine ◽  
Inflammatory Pathway ◽  
Anti Inflammatory

The Role of α7nAChR-Mediated Cholinergic Anti-inflammatory Pathway in Immune Cells

Inflammation ◽  
2021 ◽  
Author(s):  
Yi-jin Wu ◽  
Li Wang ◽  
Chao-fan Ji ◽  
Shao-fei Gu ◽  
Qin Yin ◽  
...  
Keyword(s):  
Immune Cells ◽  
Inflammatory Pathway ◽  
Anti Inflammatory

The role of the α7nAChR-mediated cholinergic anti-inflammatory pathway in Hirschsprung associated enterocolitis

2020 ◽  
Author(s):  
Feng Chen ◽  
Xiaoyu Wei ◽  
Xiaohua Chen ◽  
Lei Xiang ◽  
Xinyao Meng ◽  
...  
Keyword(s):  
Western Blotting ◽  
Mrna Level ◽  
Underlying Mechanism ◽  
Mrna Levels ◽  
Wild Type ◽  
Inflammatory Pathway ◽  
Anti Inflammatory ◽  
Phosphorylated Stat3 ◽  
Morphology Changes

Abstract Background To investigate the role and the underlying mechanism of the α7nAChR-mediated cholinergic anti-inflammatory pathway in the pathogenesis of Hirschsprung(HSCR) associated enterocolitis（HAEC）. Methods Experimental group:twenty-one-day-old Ednrb-/- mice were selected (n=10), with comparable-age wild type(Ednrb+/+) mice controls (n=10). Intestinal samples were collected. The experimental colons were divided into narrow and dilated segments according to morphology changes. The control colons were divided into distal and proximal segments.Colon HE staining was used to judge HAEC.Acetylcholine levels in colon was measured using enzyme-linked immunosorbent assays. Detected phosphorylated Jak2 (p-Jak2), Jak2, phosphorylated Stat3 (p-Stat3), Stat3, phosphorylated IκBα (p-IκBα) and IκBα were studied by Western blotting; mRNA levels of Jak2, Stat3, and IκBα were detected by RT-qPCR. Results Colon HE staining indicated that HAEC mainly occured in the dilated segments of HSCR mice (Ednrb-/- mice) (EDNRB-P).Acetylcholine content in EDNRB-P was significantly lower than that in the narrow segments (EDNRB-D) (P<0.05). Western blotting showed that the Jak2, p-Jak2, Stat3 and p-Stat3 levels in EDNRB-D were significantly higher than those in EDNRB-P (P<0.05). The p-IκBα and IκBα levels in EDNRB-P were significantly higher than those in EDNRB-D(P<0.05). The mRNA levels of Jak2 and Stat3 in EDNRB-D were higher than those in EDNRB-P, but the IκBα mRNA level was significantly lower than that in EDNRB-P (P<0.05). Conclusions During HAEC, the inflammation in the dilated segment was more severe ,while in the narrow segment there was no obvious inflammatory reaction and the content of acetylcholine was higher, which was associated with the α7nAChR-mediated cholinergic anti-inflammatory pathway.

scholarly journals Critical Role of Hypoxia and A2A Adenosine Receptors in Liver Tissue-Protecting Physiological Anti-Inflammatory Pathway

2008 ◽  
Vol 14 (3-4) ◽  
pp. 116-123 ◽  
Author(s):  
Alexander Choukèr ◽  
Manfred Thiel ◽  
Dmitriy Lukashev ◽  
Jerrold M. Ward ◽  
Ines Kaufmann ◽  
...  
Keyword(s):  
Adenosine Receptors ◽  
Liver Tissue ◽  
Critical Role ◽  
Inflammatory Pathway ◽  
A2a Adenosine Receptors ◽  
Anti Inflammatory

scholarly journals Vagal stimulation mimics preconditioning and postconditioning of ischemic myocardium in mice by activating different protection mechanisms

2018 ◽  
Vol 314 (6) ◽  
pp. H1289-H1297 ◽  
Author(s):  
Bruno Buchholz ◽  
Jazmín Kelly ◽  
Marina Muñoz ◽  
Eduardo A. Bernatené ◽  
Nahuel Méndez Diodati ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Nicotinic Receptors ◽  
Vagal Stimulation ◽  
Ischemic Myocardium ◽  
Short Term ◽  
Nicotinic Acetylcholine ◽  
Inflammatory Pathway ◽  
Myocardial Ischemia And Reperfusion ◽  
Anti Inflammatory ◽  
Gsk 3Β

Vagal stimulation (VS) during myocardial ischemia and reperfusion has beneficial effects. However, it is not known whether short-term VS applied before ischemia or at the onset of reperfusion protects the ischemic myocardium. This study was designed to determine whether short-term VS applied before ischemia or at the onset of reperfusion reduces myocardial infarct size (IS), mimicking classic preconditioning and postconditioning. A second objective was to study the participation of muscarinic and nicotinic receptors in the protection of both preischemic and reperfusion stimulation. FVB mice were subjected to 30 min of regional myocardial ischemia followed by 2 h of reperfusion without VS, with 10-min preischemic VS (pVS), or with VS during the first 10 min of reperfusion (rVS). pVS reduced IS, and this effect was abolished by atropine and wortmannin. rVS also reduced IS in a similar manner, and this effect was abolished by the α7-nicotinic acetylcholine receptor blocker methyllycaconitine. pVS increased Akt and glycogen synthase kinase (GSK)-3β phosphorylation. No changes in Akt and GSK-3β phosphorylation were observed in rVS. Stimulation-mediated IS protection was abolished with the JAK2 blocker AG490. rVS did not modify IL-6 and IL-10 levels in the plasma or myocardium. Splenic denervation and splenectomy did not abolish the protective effect of rVS. In conclusion, pVS and rVS reduced IS by different mechanisms: pVS activated the Akt/GSK-3β muscarinic pathway, whereas rVS activated α7-nicotinic acetylcholine receptors and JAK2, independently of the cholinergic anti-inflammatory pathway. NEW & NOTEWORTHY Our data suggest, for the first time, that vagal stimulation applied briefly either before ischemia or at the beginning of reperfusion mimics classic preconditioning and postconditioning and reduces myocardial infarction, activating different mechanisms. We also infer an important role of α7-nicotinic receptors for myocardial protection independent of the cholinergic anti-inflammatory pathway.

scholarly journals The anti-inflammatory pathway regulated via nicotinic acetylcholine receptors in rat intestinal mesothelial cells

2017 ◽  
Vol 79 (11) ◽  
pp. 1795-1802 ◽  
Author(s):  
Taiki MIHARA ◽  
Wataru OTSUBO ◽  
Kazuhide HORIGUCHI ◽  
Shoma MIKAWA ◽  
Noriyuki KAJI ◽  
...  
Keyword(s):  
Nicotinic Acetylcholine Receptors ◽  
Acetylcholine Receptors ◽  
Mesothelial Cells ◽  
Nicotinic Acetylcholine ◽  
Inflammatory Pathway ◽  
Anti Inflammatory

May BDNF Be Implicated in the Exercise-Mediated Regulation of Inflammation? Critical Review and Synthesis of Evidence

2014 ◽  
Vol 17 (5) ◽  
pp. 521-539 ◽  
Author(s):  
Elizabeth D. E. Papathanassoglou ◽  
Panagiota Miltiadous ◽  
Maria N. Karanikola
Keyword(s):  
Inflammatory Diseases ◽  
Inflammatory Pathway ◽  
Parasympathetic System ◽  
Bidirectional Signaling ◽  
Wide Range ◽  
System Activation ◽  
Physiological Pathways ◽  
Anti Inflammatory ◽  
Critical Literature

Introduction: Exercise attenuates inflammation and enhances levels of brain-derived neurotrophic factor (BDNF). Exercise also enhances parasympathetic tone, although its role in activating the cholinergic anti-inflammatory pathway is unclear. The physiological pathways of exercise’s effect on inflammation are obscure. Aims: To critically review the evidence on the role of BDNF in the anti-inflammatory effects of exercise and its potential involvement in the cholinergic anti-inflammatory pathway. Methods: Critical literature review of studies published in MEDLINE, PubMed, CINAHL, Embase, and Cochrane databases. Results: BDNF is critically involved in the bidirectional signaling between immune and neurosensory cells and in the regulation of parasympathetic system responses. BDNF is also intricately involved in the inflammatory response: inflammation induces BDNF production, and, in turn, BDNF exerts pro- and/or anti-inflammatory effects. Although exercise modulates BDNF and its receptors in lymphocytes, data on BDNF’s immunoregulatory/anti-inflammatory effects in relation to exercise are scarce. Moreover, BDNF increases cholinergic activity and is modulated by parasympathetic system activation. However, its involvement in the cholinergic anti-inflammatory pathway has not been investigated. Conclusion: Converging lines of evidence implicate BDNF in exercise-mediated regulation of inflammation; however, data are insufficient to draw concrete conclusions. We suggest that there is a need to investigate BDNF as a potential modulator/mediator of the anti-inflammatory effects of exercise and of the cholinergic anti-inflammatory pathway during exercise. Such research would have implications for a wide range of inflammatory diseases and for planning targeted exercise protocols.

scholarly journals A Translational Perspective of Maternal Immune Activation by SARS-CoV-2 on the Potential Prenatal Origin of Neurodevelopmental Disorders: The Role of the Cholinergic Anti-inflammatory Pathway

2021 ◽  
Vol 12 ◽  
Author(s):  
José Javier Reyes-Lagos ◽  
Eric Alonso Abarca-Castro ◽  
Juan Carlos Echeverría ◽  
Hugo Mendieta-Zerón ◽  
Alejandra Vargas-Caraveo ◽  
...  
Keyword(s):  
Immune Activation ◽  
Neurodevelopmental Disorders ◽  
Inflammatory Pathway ◽  
Maternal Immune Activation ◽  
Increased Risk ◽  
Anti Inflammatory ◽  
Psychophysiological Data

The emergent Coronavirus Disease 2019 (COVID-19) caused by the Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) could produce a maternal immune activation (MIA) via the inflammatory response during gestation that may impair fetal neurodevelopment and lead to postnatal and adulthood mental illness and behavioral dysfunctions. However, so far, limited evidence exists regarding long-term physiological, immunological, and neurodevelopmental modifications produced by the SARS-CoV-2 in the human maternal-fetal binomial and, particularly, in the offspring. Relevant findings derived from epidemiological and preclinical models show that a MIA is indeed linked to an increased risk of neurodevelopmental disorders in the offspring. We hypothesize that a gestational infection triggered by SARS-CoV-2 increases the risks leading to neurodevelopmental disorders of the newborn, which can affect childhood and the long-term quality of life. In particular, disruption of either the maternal or the fetal cholinergic anti-inflammatory pathway (CAP) could cause or exacerbate the severity of COVID-19 in the maternal-fetal binomial. From a translational perspective, in this paper, we discuss the possible manifestation of a MIA by SARS-CoV-2 and the subsequent neurodevelopmental disorders considering the role of the fetal-maternal cytokine cross-talk and the CAP. Specifically, we highlight the urgent need of preclinical studies as well as multicenter and international databanks of maternal-fetal psychophysiological data obtained pre-, during, and post-infection by SARS-CoV-2 from pregnant women and their offspring.

scholarly journals Systemic Administration of α7-Nicotinic Acetylcholine Receptor Ligands Does Not Improve Renal Injury or Behavior in Mice With Advanced Systemic Lupus Erythematosus

2021 ◽  
Vol 8 ◽  
Author(s):  
Jessica Y. Morales ◽  
Cassandra M. Young-Stubbs ◽  
Caroline G. Shimoura ◽  
William R. Kem ◽  
Victor V. Uteshev ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Nicotinic Acetylcholine Receptor ◽  
Lupus Erythematosus ◽  
Advanced Disease ◽  
Organ Damage ◽  
Systemic Lupus ◽  
Nicotinic Acetylcholine ◽  
Inflammatory Pathway ◽  
Α7 Nachr ◽  
Anti Inflammatory

There is a critical need for safe treatment options to control inflammation in patients with systemic lupus erythematosus (SLE) since the inflammation contributes to morbidity and mortality in advanced disease. Endogenous neuroimmune mechanisms like the cholinergic anti-inflammatory pathway can be targeted to modulate inflammation, but the ability to manipulate such pathways and reduce inflammation and end organ damage has not been fully explored in SLE. Positive allosteric modulators (PAM) are pharmacological agents that inhibit desensitization of the nicotinic acetylcholine receptor (α7-nAChR), the main anti-inflammatory feature within the cholinergic anti-inflammatory pathway, and may augment α7-dependent cholinergic tone to generate therapeutic benefits in SLE. In the current study, we hypothesize that activating the cholinergic anti-inflammatory pathway at the level of the α7-nAChR with systemic administration of a partial agonist, GTS-21, and a PAM, PNU-120596, would reduce inflammation, eliminating the associated end organ damage in a mouse model of SLE with advanced disease. Further, we hypothesize that systemic α7 ligands will have central effects and improve behavioral deficits in SLE mice. Female control (NZW) and SLE mice (NZBWF1) were administered GTS-21 or PNU-120596 subcutaneously via minipumps for 2 weeks. We found that the increased plasma dsDNA autoantibodies, splenic and renal inflammation, renal injury and hypertension usually observed in SLE mice with advanced disease at 35 weeks of age were not altered by GTS-21 or PNU-120596. The anxiety-like behavior presented in SLE mice was also not improved by GTS-21 or PNU-120596. Although no significant beneficial effects of α7 ligands were observed in SLE mice at this advanced stage, we predict that targeting this receptor earlier in the pathogenesis of the disease may prove to be efficacious and should be addressed in future studies.

Sign in / Sign up

Export Citation Format

Share Document