Regulatory effect of nicotine on collagen-induced arthritis and on the induction and function of in vitro-cultured Th17 cells

Yang, Yiming; Yang, Yan; Yang, Jie; Xie, Ruiqin; Ren, Yana; Fan, Huimin

doi:10.3109/14397595.2013.862352

Cited by 10 publications

(8 citation statements)

References 27 publications

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“…Stimulation of the a7nAChR with nicotine or AR-R17779 resulted in reduced clinical arthritis scores and decreased expression of TNF [40]. Other studies confirmed these results using the a7nAChR agonist GTS-21 (also known as dimethoxybenzylidene anabaseine, DMBX-A) or nicotine [40,[61][62][63]. Conversely, unilateral dissection of the vagus nerve resulted in a trend towards increased arthritis activity in animal models of arthritis which did not reach statistical significance, possibly due to the relatively small number of animals tested [40,62].…”

Section: Influence Of the Autonomic Nervous System On Chronic Inflammsupporting

confidence: 73%

Balancing the autonomic nervous system to reduce inflammation in rheumatoid arthritis

et al. 2017

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Imbalance in the autonomic nervous system (ANS) has been observed in many established chronic autoimmune diseases, including rheumatoid arthritis (RA), which is a prototypic immune‐mediated inflammatory disease (IMID). We recently discovered that autonomic dysfunction precedes and predicts arthritis development in subjects at risk of developing seropositive RA. In addition, RA patients with relatively high vagus nerve tone (higher parasympathetic parameters, measured by heart rate variability) respond better to antirheumatic therapies. Together, these data suggest that the ANS may control inflammation in humans. This notion is supported by experimental studies in animal models of RA. We have found that stimulation of the so‐called cholinergic anti‐inflammatory pathway by efferent electrical vagus nerve stimulation (VNS) or pharmacological activation of the alpha7 subunit of nicotinic acetylcholine receptors (α7nAChR) improves clinical signs and symptoms of arthritis, reduces cytokine production and protects against progressive joint destruction. Conversely, increased arthritis activity was observed in alpha7nAChR knockout mice. These studies together with previous work in animal models of sepsis and other forms of inflammation provided the rationale for an experimental clinical trial in patients with RA. We could for the first time show that an implantable vagus nerve stimulator inhibits peripheral blood cytokine production in humans. VNS significantly inhibited TNF and IL‐6 production and improved RA disease severity, even in some patients with therapy‐resistant disease. This work strongly supports further studies using a bioelectronic approach to treat RA and other IMIDs.

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Section: Influence Of the Autonomic Nervous System On Chronic Inflammsupporting

confidence: 73%

Balancing the autonomic nervous system to reduce inflammation in rheumatoid arthritis

et al. 2017

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“…The cholinergic anti-inflammatory pathway is the efferent or motor arm of the "inflammatory reflex", the neural circuit that responds to and regulates the inflammatory response (15). In the neural circuit, the neurotransmitter endogenic acetylcholine, for example, can interact with the receptors expressed on immune cells and thus alter immune cell function (16). It is generally acknowledged that acetylcholine can bind to the integral membrane protein as acetylcholine receptors, including nicotinic acetylcholine receptors (nAChR) and muscarinic acetylcholine receptors (mAChR).…”

Section: Nicotine and Inflammationmentioning

confidence: 99%

“…Until day 35, the nicotine group significantly suppressed histological IL-17A, serum TNFa, and pro-inflammatory cytokines IL-17A and IL-6 mRNA expression in isolated splenocytes. Furthermore, isolated CD4 + IL-17A + Th17 cells expressing a7 nAChR stimulated by nicotine may decrease their pro-inflammatory function (16). Nicotine was added to drinking water (100 mg/ml, about 300 mg nicotine per day per mouse) for male DBA/1 mice from the day of immunization by chicken collagen II, resulting in a delay in arthritis.…”

Section: Anti-inflammatory Effect Of Nicotine On Arthritismentioning

confidence: 99%

Nicotine in Inflammatory Diseases: Anti-Inflammatory and Pro-Inflammatory Effects

et al. 2022

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As an anti-inflammatory alkaloid, nicotine plays dual roles in treating diseases. Here we reviewed the anti-inflammatory and pro-inflammatory effects of nicotine on inflammatory diseases, including inflammatory bowel disease, arthritis, multiple sclerosis, sepsis, endotoxemia, myocarditis, oral/skin/muscle inflammation, etc., mainly concerning the administration methods, different models, therapeutic concentration and duration, and relevant organs and tissues. According to the data analysis from recent studies in the past 20 years, nicotine exerts much more anti-inflammatory effects than pro-inflammatory ones, especially in ulcerative colitis, arthritis, sepsis, and endotoxemia. On the other hand, in oral inflammation, nicotine promotes and aggravates some diseases such as periodontitis and gingivitis, especially when there are harmful microorganisms in the oral cavity. We also carefully analyzed the nicotine dosage to determine its safe and effective range. Furthermore, we summarized the molecular mechanism of nicotine in these inflammatory diseases through regulating immune cells, immune factors, and the vagus and acetylcholinergic anti-inflammatory pathways. By balancing the “beneficial” and “harmful” effects of nicotine, it is meaningful to explore the effective medical value of nicotine and open up new horizons for remedying acute and chronic inflammation in humans.

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“…For example, nicotinic agonists induce T-helper cells shift to a Th2 anti-inflammatory phenotype [75]. Nicotine can also inhibit inflammation in arthritis by reducing IL-17 production by splenic α7nAChR-expressing Th17 cells [76], or preventing macrophage infiltration into the synovial tissues by inhibiting the expression of adhesion molecules such as ICAM-1 [77]. Indeed, RA was originally considered a Th1-mediated disease due to the high levels of TNF and IFN-γ and the lack of Th2-cytokines such as IL-4.…”

Section: Pharmacological Translation For Arthritismentioning

confidence: 99%

From Neuroimunomodulation to Bioelectronic Treatment of Rheumatoid Arthritis

et al. 2018

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Neuronal stimulation is an emerging field in modern medicine to control organ function and reestablish physiological homeostasis during illness. The nervous system innervates most of the peripheral organs and provides a fine tune to control the immune system. Most of these studies have focused on vagus nerve stimulation and the physiological, cellular and molecular mechanisms regulating the immune system. Here, we review the new results revealing afferent vagal signaling pathways, immunomodulatory brain structures, spinal cord-dependent circuits, neural and non-neural cholinergic/catecholaminergic signals and their respective receptors contributing to neuromodulation of inflammation in rheumatoid arthritis. These new neuromodulatory networks and structures will allow the design of innovative bioelectronic or pharmacological approaches for safer and low-cost treatment of arthritis and related inflammatory disorders.

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Regulatory effect of nicotine on collagen-induced arthritis and on the induction and function of in vitro-cultured Th17 cells

Abstract: Nicotine stimulation attenuated signs and severity of arthritis in mice. Activation of nicotine acetylcholine receptors on in vitro-cultured Th17 cells decreased their pro-inflammatory function, which may play a potential role in alleviating arthritis in mice.

Cited by 10 publications

References 27 publications

Balancing the autonomic nervous system to reduce inflammation in rheumatoid arthritis

Balancing the autonomic nervous system to reduce inflammation in rheumatoid arthritis

Nicotine in Inflammatory Diseases: Anti-Inflammatory and Pro-Inflammatory Effects

From Neuroimunomodulation to Bioelectronic Treatment of Rheumatoid Arthritis

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