Lipid-rich enteral nutrition regulates mucosal mast cell activation via the vagal anti-inflammatory reflex.

J. de Haan, M. Hadfoune, T. Lubbers, C.M.I. Hodin, K. Lenaerts, A. Ito, I.Y. Verbaeys, M.J. Skynner, C. Cailotto, J. van der Vliet, W.J. de Jonge, J.W. Greve, W.A. Buurman

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Abstract

Nutritional stimulation of the cholecystokinin-1 receptor (CCK-1R) and acetylcholine receptor (nAChR)-mediated vagal reflex was shown to reduce inflammation and preserve intestinal integrity. Mast cells are important effectors of the innate immune response, therefore modulation of mucosal cells is a potential therapeutic target to control the acute response in the intestine. The present study investigates intestinal responsiveness upon nutritional activation of the vagal anti- during acute inflammation. Mucosal mast cell degranulation was induced mice by administration of Salmonella enterica LPS. Lipid-rich enteral prior to LPS significantly decreased circulatory levels of mouse mast protease at 30 minutes post-LPS compared with isocaloric low-lipid fasting. CCK-1R blockage reversed the inhibitory effects of lipid-rich whereas stimulation of the peripheral CCK-1R mimicked nutritional mast inhibition. The effects of lipid-rich nutrition were negated by nAChR chlorisondamine and alpha-bungarotoxin and vagal intestinal denervation. release of beta-hexosaminidase by MC/9 mast cells following LPS or IgE- complexes was dose-dependently inhibited by acetylcholine and nicotine. Application of GSK1345038A, a specific agonist of the nAChR alpha7, in marrow derived mast cells from nAChR beta2-/- and wild types indicated cholinergic inhibition of mast cells is mediated by the nAChR alpha7 and independent of the nAChR beta2. Together, the current study reveals cells as a previously unknown target of the nutritional anti- reflex.
Original languageEnglish
Pages (from-to)G383-G391
JournalAmerican Journal of Physiology-Gastrointestinal and Liver Physiology
Volume305
Issue number5
DOIs
Publication statusPublished - 1 Jan 2013

Cite this

de Haan, J. ; Hadfoune, M. ; Lubbers, T. ; Hodin, C.M.I. ; Lenaerts, K. ; Ito, A. ; Verbaeys, I.Y. ; Skynner, M.J. ; Cailotto, C. ; van der Vliet, J. ; de Jonge, W.J. ; Greve, J.W. ; Buurman, W.A. / Lipid-rich enteral nutrition regulates mucosal mast cell activation via the vagal anti-inflammatory reflex. In: American Journal of Physiology-Gastrointestinal and Liver Physiology. 2013 ; Vol. 305, No. 5. pp. G383-G391.
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title = "Lipid-rich enteral nutrition regulates mucosal mast cell activation via the vagal anti-inflammatory reflex.",
abstract = "Nutritional stimulation of the cholecystokinin-1 receptor (CCK-1R) and acetylcholine receptor (nAChR)-mediated vagal reflex was shown to reduce inflammation and preserve intestinal integrity. Mast cells are important effectors of the innate immune response, therefore modulation of mucosal cells is a potential therapeutic target to control the acute response in the intestine. The present study investigates intestinal responsiveness upon nutritional activation of the vagal anti- during acute inflammation. Mucosal mast cell degranulation was induced mice by administration of Salmonella enterica LPS. Lipid-rich enteral prior to LPS significantly decreased circulatory levels of mouse mast protease at 30 minutes post-LPS compared with isocaloric low-lipid fasting. CCK-1R blockage reversed the inhibitory effects of lipid-rich whereas stimulation of the peripheral CCK-1R mimicked nutritional mast inhibition. The effects of lipid-rich nutrition were negated by nAChR chlorisondamine and alpha-bungarotoxin and vagal intestinal denervation. release of beta-hexosaminidase by MC/9 mast cells following LPS or IgE- complexes was dose-dependently inhibited by acetylcholine and nicotine. Application of GSK1345038A, a specific agonist of the nAChR alpha7, in marrow derived mast cells from nAChR beta2-/- and wild types indicated cholinergic inhibition of mast cells is mediated by the nAChR alpha7 and independent of the nAChR beta2. Together, the current study reveals cells as a previously unknown target of the nutritional anti- reflex.",
author = "{de Haan}, J. and M. Hadfoune and T. Lubbers and C.M.I. Hodin and K. Lenaerts and A. Ito and I.Y. Verbaeys and M.J. Skynner and C. Cailotto and {van der Vliet}, J. and {de Jonge}, W.J. and J.W. Greve and W.A. Buurman",
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Lipid-rich enteral nutrition regulates mucosal mast cell activation via the vagal anti-inflammatory reflex. / de Haan, J.; Hadfoune, M.; Lubbers, T.; Hodin, C.M.I.; Lenaerts, K.; Ito, A.; Verbaeys, I.Y.; Skynner, M.J.; Cailotto, C.; van der Vliet, J.; de Jonge, W.J.; Greve, J.W.; Buurman, W.A.

In: American Journal of Physiology-Gastrointestinal and Liver Physiology, Vol. 305, No. 5, 01.01.2013, p. G383-G391.

Research output: Contribution to journalArticleAcademicpeer-review

TY - JOUR

T1 - Lipid-rich enteral nutrition regulates mucosal mast cell activation via the vagal anti-inflammatory reflex.

AU - de Haan, J.

AU - Hadfoune, M.

AU - Lubbers, T.

AU - Hodin, C.M.I.

AU - Lenaerts, K.

AU - Ito, A.

AU - Verbaeys, I.Y.

AU - Skynner, M.J.

AU - Cailotto, C.

AU - van der Vliet, J.

AU - de Jonge, W.J.

AU - Greve, J.W.

AU - Buurman, W.A.

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N2 - Nutritional stimulation of the cholecystokinin-1 receptor (CCK-1R) and acetylcholine receptor (nAChR)-mediated vagal reflex was shown to reduce inflammation and preserve intestinal integrity. Mast cells are important effectors of the innate immune response, therefore modulation of mucosal cells is a potential therapeutic target to control the acute response in the intestine. The present study investigates intestinal responsiveness upon nutritional activation of the vagal anti- during acute inflammation. Mucosal mast cell degranulation was induced mice by administration of Salmonella enterica LPS. Lipid-rich enteral prior to LPS significantly decreased circulatory levels of mouse mast protease at 30 minutes post-LPS compared with isocaloric low-lipid fasting. CCK-1R blockage reversed the inhibitory effects of lipid-rich whereas stimulation of the peripheral CCK-1R mimicked nutritional mast inhibition. The effects of lipid-rich nutrition were negated by nAChR chlorisondamine and alpha-bungarotoxin and vagal intestinal denervation. release of beta-hexosaminidase by MC/9 mast cells following LPS or IgE- complexes was dose-dependently inhibited by acetylcholine and nicotine. Application of GSK1345038A, a specific agonist of the nAChR alpha7, in marrow derived mast cells from nAChR beta2-/- and wild types indicated cholinergic inhibition of mast cells is mediated by the nAChR alpha7 and independent of the nAChR beta2. Together, the current study reveals cells as a previously unknown target of the nutritional anti- reflex.

AB - Nutritional stimulation of the cholecystokinin-1 receptor (CCK-1R) and acetylcholine receptor (nAChR)-mediated vagal reflex was shown to reduce inflammation and preserve intestinal integrity. Mast cells are important effectors of the innate immune response, therefore modulation of mucosal cells is a potential therapeutic target to control the acute response in the intestine. The present study investigates intestinal responsiveness upon nutritional activation of the vagal anti- during acute inflammation. Mucosal mast cell degranulation was induced mice by administration of Salmonella enterica LPS. Lipid-rich enteral prior to LPS significantly decreased circulatory levels of mouse mast protease at 30 minutes post-LPS compared with isocaloric low-lipid fasting. CCK-1R blockage reversed the inhibitory effects of lipid-rich whereas stimulation of the peripheral CCK-1R mimicked nutritional mast inhibition. The effects of lipid-rich nutrition were negated by nAChR chlorisondamine and alpha-bungarotoxin and vagal intestinal denervation. release of beta-hexosaminidase by MC/9 mast cells following LPS or IgE- complexes was dose-dependently inhibited by acetylcholine and nicotine. Application of GSK1345038A, a specific agonist of the nAChR alpha7, in marrow derived mast cells from nAChR beta2-/- and wild types indicated cholinergic inhibition of mast cells is mediated by the nAChR alpha7 and independent of the nAChR beta2. Together, the current study reveals cells as a previously unknown target of the nutritional anti- reflex.

U2 - 10.1152/ajpgi.00333.2012

DO - 10.1152/ajpgi.00333.2012

M3 - Article

VL - 305

SP - G383-G391

JO - American Journal of Physiology-Gastrointestinal and Liver Physiology

JF - American Journal of Physiology-Gastrointestinal and Liver Physiology

SN - 0193-1857

IS - 5

ER -