Abstract
BackgroundThe vagus nerve has emerged as an important modulator of the intestinal immune system. Its anti‐inflammatory properties have been previously shown in innate and Th1/Th17 predominant inflammatory models. To what extent the vagus nerve is of importance in Th2 inflammatory responses like food allergy is still unclear. In this study, we therefore aimed to investigate the effect of vagotomy (VGX) and vagus nerve stimulation (VNS), on the development and severity of experimental food allergy.MethodsBalb/C mice were first sensitized with ovalbumin (OVA) in the presence of alum. Prior to oral challenges with OVA, mice were subjected to VGX or VNS. Disease severity was determined by assessing severity and onset of diarrhoea, OVA‐specific antibody production, mast cell number and activity, inflammatory gene expression in duodenal tissue and lamina propria immune cells by flow cytometry analysis.ResultsWhen compared to control mice, VGX did not significantly affect the development and severity of the disease in our model of food allergy. VNS, on the other hand, resulted in a significant amelioration of the different inflammatory parameters assessed. This effect was independent of α7nAChR and is possibly mediated through the dampening of mast cells and increased phagocytosis of OVA by CX3CR1hi macrophages.ConclusionsThese results underscore the anti‐inflammatory properties of the vagus nerve and the potential of neuro‐immune interactions in the intestine. Further insight into the underlying mechanisms could ultimately lead to novel therapeutic approaches in the treatment of not only food allergy but also other immune‐mediated diseases.
Highlights
Food allergy has been on the rise in westernized countries for several decades with numbers reportedly rising up to ap‐ proximately 10%
ILC2s and Th2 cells in the small intestine (SI) lamina propria (LP) of vagus nerve stimulation (VNS)‐ and sham‐stimulated mice revealed no significant differences in eosinophils, ILC2s and Th2 cells
Due to its proven anti‐inflammatory properties and dense innerva‐ tion of the gut, the vagus nerve (VN) has become a major topic of interest in the treatment of several gastrointestinal disorders
Summary
Food allergy has been on the rise in westernized countries for several decades with numbers reportedly rising up to ap‐ proximately 10%. In 2000, Tracey et al[5] introduced the “inflammatory reflex,” showing the ability of the vagus nerve (VN) to sense peripheral inflammation and inform the brain on the inflammatory status to subsequently dampen the inflammatory response This con‐ cept was later translated to the gastrointestinal tract, showing that vagal nerve stimulation (VNS) reduced inflammation of the intestinal muscle layer and restored gastrointestinal transit in a model of postoperative ileus.[6] it was demonstrated this effect is exerted by activation of enteric cholinergic neurons interacting with resident muscular CX3CR1hi macrophages via α7 nicotinic acetylcholine receptors (α7nAChR).[7] To date, several additional studies have evaluated the effect of VNS and pharma‐ cological cholinergic modulation in a range of experimental inflam‐ matory models including endotoxemia, sepsis, inflammatory bowel disease, obesity and arthritis.[8,9,10,11,12,13,14]. Elucidating a potential role for cholin‐ ergic modulation in type 2‐mediated food allergy could provide novel insights to increase our understanding in the pathogenesis of food allergy and lead to development of new treat‐ ment options for food allergy
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