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Nerve stimulation promotes resolution of inflammation – Neuroscience News

Summary: Electrical stimulation of the vagus nerve promotes healing in people with acute inflammation by altering the balance between inflammatory and anti-inflammatory molecules.

source: Karolinska Institute

The nervous system is known to communicate with the immune system and regulate inflammation in the body. Researchers at the Karolinska Institutet in Sweden are now showing how electrical stimulation of a specific nerve can promote healing in acute inflammatory conditions.

The result was published in the magazine PNASopens up new ways to speed up the resolution of inflammation.

The way the body regulates inflammation is not partially understood. Previous research by Peder Olofsson at the Karolinska Institutet and other research groups has shown that electrical stimulation of the vagus nerve can reduce inflammation.

This nerve stimulation has been used with encouraging results in clinical studies of patients with inflammatory bowel disease and rheumatoid arthritis. However, it has not been clear how nerve signals regulate the active resolution of inflammation.

“We have now studied the effects of signaling between nerves and immune cells at the molecular level,” Karavaca, researcher in Peder Olofsson’s group at the Department of Medicine, Solna, Karolinska Institutet and Stockholm Center for Bioelectronic Medicine at MedTechLabs. .

“A better understanding of these mechanisms will allow for more precise applications that harness the nervous system to regulate inflammation.”

Researchers have shown that electrical stimulation of the vagus nerve in an inflamed state alters the balance between specialized anti-inflammatory and anti-inflammatory molecules, promoting healing.

“Inflammation and its translucency play a major role in a wide range of common diseases, including autoimmune disease and cardiovascular disease,” says Peder Olofsson.

“Our findings provide insights into how the nervous system can speed up the resolution of inflammation by activating specific signaling pathways.”

Researchers will continue to study how nerves regulate inflammation healing in more detail. The image is in the public domain

Researchers will continue to study how nerves regulate inflammation healing in more detail.

“The vagus nerve is just one of many nerves that regulate the immune system. We will continue to map the networks of nerves that regulate inflammation at the molecular level and study how these signals participate in disease progression,” says Dr. Olofson.

“We hope this research will provide a better understanding of how to treat pathological inflammation, and contribute to more effective treatments for many inflammatory diseases, such as atherosclerosis and rheumatism.”

Financing: The study was supported by grants from the Knut and Alice Wallenberg Foundation, the Swedish Research Council, the Swedish Heart-Lung Foundation, MedTechLabs and Novo Nordisk. Peder Olofsson owns shares in Emune AB. Co-author Jesmond Daly is founder and chief research officer of Resolomics Ltd.

About this research Brain stimulation and inflammation News

author: press office
source: Karolinska Institute
Contact: Press Office – Karolinska Institutet
picture: The image is in the public domain

original search: Access closed.
“Stimulation of the vagus nerve enhances resolution of inflammation by a mechanism that involves Alox15 and requires the α7nAChR subunit” by April S. Caravaca et al. PNAS


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Stimulation of the vagus nerve promotes resolution of inflammation through a mechanism that involves Alox15 and requires the α7nAChR . subunit

The causes of non-resolving inflammation lie in a group of chronic inflammatory diseases, and therapeutic acceleration of inflammation resolution may improve outcomes.

Neurological reactions regulate the intensity of inflammation (eg, through signals in the vagus nerve), but whether vagus nerve activation promotes resolution of inflammation in vivo is unknown.

To investigate this, mice were subjected to electrical vagus nerve stimulation (VNS) or sham surgery at the cervical level followed by zymosan-induced peritonitis.

The duration of inflammation resolution was significantly reduced and B-cell polymorphism was significantly increased in VNS-treated mice compared with the sham images. Lipid mediator (LM) metabolites revealed that VNS-treated mice had higher levels of pre-specialized mediators (SPMs), particularly of the omega-3 metabolites docosahexaenoic (DHA) and docosapentaenoic (n-3 DPA), in peritoneal secretions.

VNS also shifted the ratio between proinflammatory and proinflammatory LMs towards a porous profile, but this effect was reversed by VNS in mice deficient in 12/15-lipoxgenase (Alox15), a key enzyme in SPM biosynthesis.

The significant VNS-mediated reduction of neutrophil numbers in peritoneal secretions was absent in mice deficient in the α7-nicotinic acetylcholine receptor (α7nAChR) subunit, an essential component of the inflammatory reversal.

Thus, VNS increased local levels of SPM and accelerated the resolution of inflammation in zymosan-induced peritonitis through a mechanism involving Alox15 and requiring α7nAChR.

2022-05-31 19:47:34

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