Effects of anti-inflammatory vagus nerve stimulation in endotoxemic rats on blood and spleen lymphocyte subsets

Mihaylova, Stanka; Schweighöfer, Hanna; Hackstein, Holger; Rosengarten, Bernhard

doi:10.1007/s00011-014-0741-5

Cited by 20 publications

(9 citation statements)

References 39 publications

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“…It would be of interest to specifically evaluate the relationship between the number of baseline acetylcholine‐producing T‐cells and improvement in fatigue scores in response to nVNS. Given that it takes several hours for cell division to take place, the increased numbers of T‐cells, NK‐cells, and NKT‐cells after the first nVNS dose is more likely a consequence of the marginalization of these immune cells after nVNS , or the redistribution of cell subsets in different compartments.…”

Section: Discussionmentioning

confidence: 99%

The Effects of Noninvasive Vagus Nerve Stimulation on Fatigue and Immune Responses in Patients With Primary Sjögren’s Syndrome

Tarn

Legg

Mitchell

et al. 2019

Neuromodulation: Technology at the Neural Interface

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Section: Discussionmentioning

confidence: 99%

The Effects of Noninvasive Vagus Nerve Stimulation on Fatigue and Immune Responses in Patients With Primary Sjögren’s Syndrome

Tarn

Legg

Mitchell

et al. 2019

Neuromodulation: Technology at the Neural Interface

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“…In the present study, we aimed to extend our previous research on vagal anti-inflammatory properties [ 13 , 14 ] to its effects on brain regions with (cortex) or without (hypothalamus) a tight blood-brain barrier. Therefore, several immune-to-brain signaling pathways (humoral and cellular) and different target structures related to the neurovascular coupling mechanism were studies in this well-established endotoxic lipopolysaccharide (LPS) sepsis model.…”

Section: Introductionmentioning

confidence: 99%

Modulatory effects of vagal stimulation on neurophysiological parameters and the cellular immune response in the rat brain during systemic inflammation

Schweighöfer

Rummel

Roth

et al. 2016

ICMx

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BackgroundStimulation of the vagus nerve has modulating, anti-inflammatory effects on the cellular immune response in the blood and the spleen, stabilizing brain function. Here, we aimed to investigate its potential effects on immune-to-brain communication focusing on neurophysiological readouts and leukocyte migration to the brain during severe sepsis-like endotoxemia.MethodsSystemic inflammation was induced by intravenous administration of lipopolysaccharide (LPS; 5 mg/kg). Animals received either no manipulation of the vagus nerve, vagotomy, or vagotomy plus vagus nerve stimulation of the distal trunk. Somatosensory evoked potentials and evoked flow velocity response were measured for 4.5 h as indicators of brain function and neurovascular coupling, respectively. In addition, brain areas with (cortex) and without (hypothalamus) tight blood-brain barrier were studied separately using immunohistochemistry and RT-PCR. Moreover, plasma cytokine and leptin levels were analyzed by ELISA.ResultsLPS induced a decline of both neurophysiological parameters, which was prevented by vagus nerve stimulation. As for peripheral organs, LPS-stimulated neutrophil counts increased in the brain and colocalized in the brain with endothelial intercellular adhesion molecule (ICAM)-1. Interestingly, vagal stimulation reduced this colocalization and decreased nuclear translocation of the brain cell activation marker nuclear factor interleukin 6 (NF-IL6). Furthermore, it reduced the gene expression of inflammatory markers and extravasation signals (IL-6, CXCL-1, ICAM-1) in the hypothalamus but not the cortex linked to a moderate decrease in circulating cytokine levels (interleukin 6, tumor necrosis factor alpha) as well as lower plasma leptin concentration.ConclusionsOur data suggest beneficial effects of anti-inflammatory vagus nerve stimulation on brain function by reducing the interaction of neurotrophil granulocytes with the brain endothelium as well as attenuating inflammatory responses in brain areas lacking a blood-brain barrier.Electronic supplementary materialThe online version of this article (doi:10.1186/s40635-016-0091-4) contains supplementary material, which is available to authorized users.

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“…In addtion, vagotomy may influence the recruitment and activity of immune cell to participate in inflammation. Mihaylova and his colleagues found vagotomy strongly decline immune cell counts (including CD4 + T cells and CD8 + T cells) in the septic spleen ( Mihaylova et al, 2014 ). The previous experiments elucidated that efferent vagal activity can significantly regulate both local and systemic inflammation.…”

Section: Discussionmentioning

confidence: 99%

Right Cervical Vagotomy Aggravates Viral Myocarditis in Mice Via the Cholinergic Anti-inflammatory Pathway

Li‐Sha

Chen

et al. 2017

Front. Pharmacol.

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The autonomic nervous system dysfunction with increased sympathetic activity and withdrawal of vagal activity may play an important role in the pathogenesis of viral myocarditis. The vagus nerve can modulate the immune response and control inflammation through a ‘cholinergic anti-inflammatory pathway’ dependent on the α7-nicotinic acetylcholine receptor (α7nAChR). Although the role of β-adrenergic stimulation on viral myocarditis has been investigated in our pervious studies, the direct effect of vagal tone in this setting has not been yet studied. Therefore, in the present study, we investigated the effects of cervical vagotomy in a murine model of viral myocarditis. In a coxsackievirus B3 murine myocarditis model (Balb/c), effects of right cervical vagotomy and nAChR agonist nicotine on echocardiography, myocardial histopathology, viral RNA, and proinflammatory cytokine levels were studied. We found that right cervical vagotomy inhibited the cholinergic anti-inflammatory pathway, aggravated myocardial lesions, up-regulated the expression of TNF-α, IL-1β, and IL-6, and worsened the impaired left ventricular function in murine viral myocarditis, and these changes were reversed by co-treatment with nicotine by activating the cholinergic anti-inflammatory pathway. These results indicate that vagal nerve plays an important role in mediating the anti-inflammatory effect in viral myocarditis, and that cholinergic stimulation with nicotine also plays its peripheral anti-inflammatory role relying on α7nAChR, without requirement for the integrity of vagal nerve in the model. The findings suggest that vagus nerve stimulation mediated inhibition of the inflammatory processes likely provide important benefits in myocarditis treatment.

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Effects of anti-inflammatory vagus nerve stimulation in endotoxemic rats on blood and spleen lymphocyte subsets

Cited by 20 publications

References 39 publications

The Effects of Noninvasive Vagus Nerve Stimulation on Fatigue and Immune Responses in Patients With Primary Sjögren’s Syndrome

The Effects of Noninvasive Vagus Nerve Stimulation on Fatigue and Immune Responses in Patients With Primary Sjögren’s Syndrome

Modulatory effects of vagal stimulation on neurophysiological parameters and the cellular immune response in the rat brain during systemic inflammation

Right Cervical Vagotomy Aggravates Viral Myocarditis in Mice Via the Cholinergic Anti-inflammatory Pathway

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