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Vagus Nerve Stimulation dampens intestinal inflammation in a murine model of experimental Food Allergy.

Tijdschriftbijdrage - Tijdschriftartikel

Background: The vagus nerve has emerged as an important modulator of the intesti‐nal 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.Methods: Balb/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.Results: When compared to control mice, VGX did not significantly affect the devel‐opment 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.Conclusions: These 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 ap‐proaches in the treatment of not only food allergy but also other immune‐mediated diseases.
Tijdschrift: ALLERGY
ISSN: 0105-4538
Issue: 9
Volume: 74
Pagina's: 1748 - 1759
Jaar van publicatie:2019
BOF-keylabel:ja
IOF-keylabel:ja
BOF-publication weight:6
CSS-citation score:2
Authors from:Higher Education
Toegankelijkheid:Open