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http://hdl.handle.net/1942/33139
Title: | Local immune response to food antigens drives meal-induced abdominal pain | Authors: | Aguilera-Lizarraga, Javier Florens, Morgane V Viola, Maria Francesca Jain, Piyush Decraecker, Lisse Appeltans, Iris Cuende-Estevez, Maria Fabre, Naomi Van Beek, Kim Perna, Eluisa Balemans, Dafne Stakenborg, Nathalie Theofanous, Stavroula Bosmans , Goele Mondelaers, Stéphanie U Matteoli, Gianluca Ibiza Martínez, Sales Lopez-Lopez, Cintya Jaramillo-Polanco, Josue Talavera, Karel AGUIAR ALPIZAR, Yeranddy Feyerabend, Thorsten B Rodewald, Hans-Reimer Farre, Ricard Redegeld, Frank A Si, Jiyeon Raes, Jeroen Breynaert, Christine Schrijvers, Rik Bosteels, Cédric Lambrecht, Bart N Boyd, Scott D Hoh, Ramona A Cabooter, Deirdre Nelis, Maxim Augustijns, Patrick HENDRIX, Sven Strid, Jessica Bisschops, Raf Reed, David E Vanner, Stephen J Denadai-Souza, Alexandre Wouters, Mira M Boeckxstaens, Guy E |
Issue Date: | 2021 | Publisher: | NATURE RESEARCH | Source: | Nature (London), 590 (7844), p. 151-156 | Abstract: | Up to 20% of people worldwide develop gastrointestinal symptoms following a meal1, leading to decreased quality of life, substantial morbidity and high medical costs. Although the interest of both the scientific and lay communities in this issue has increased markedly in recent years, with the worldwide introduction of gluten-free and other diets, the underlying mechanisms of food-induced abdominal complaints remain largely unknown. Here we show that a bacterial infection and bacterial toxins can trigger an immune response that leads to the production of dietary-antigen-specific IgE antibodies in mice, which are limited to the intestine. Following subsequent oral ingestion of the respective dietary antigen, an IgE- and mast-cell-dependent mechanism induced increased visceral pain. This aberrant pain signalling resulted from histamine receptor H1-mediated sensitization of visceral afferents. Moreover, injection of food antigens (gluten, wheat, soy and milk) into the rectosigmoid mucosa of patients with irritable bowel syndrome induced local oedema and mast cell activation. Our results identify and characterize a peripheral mechanism that underlies food-induced abdominal pain, thereby creating new possibilities for the treatment of irritable bowel syndrome and related abdominal pain disorders. | Keywords: | Experimental models of disease;Irritable bowel syndrome;Neuroimmunology;Peripheral tolerance;Translational research | Document URI: | http://hdl.handle.net/1942/33139 | ISSN: | 0028-0836 | e-ISSN: | 1476-4687 | DOI: | 10.1038/s41586-020-03118-2 | ISI #: | 000607492400003 | Category: | A1 | Type: | Journal Contribution | Validations: | ecoom 2022 |
Appears in Collections: | Research publications |
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s41586-020-03118-2.pdf Restricted Access | Published version | 16.93 MB | Adobe PDF | View/Open Request a copy |
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