{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,30]],"date-time":"2026-01-30T07:06:14Z","timestamp":1769756774367,"version":"3.49.0"},"reference-count":56,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2026,1,28]],"date-time":"2026-01-28T00:00:00Z","timestamp":1769558400000},"content-version":"vor","delay-in-days":27,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2026,1,1]],"date-time":"2026-01-01T00:00:00Z","timestamp":1767225600000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100003130","name":"Fonds Wetenschappelijk Onderzoek","doi-asserted-by":"publisher","award":["G059822N"],"award-info":[{"award-number":["G059822N"]}],"id":[{"id":"10.13039\/501100003130","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100003130","name":"Fonds Wetenschappelijk Onderzoek","doi-asserted-by":"publisher","award":["12B1B24N"],"award-info":[{"award-number":["12B1B24N"]}],"id":[{"id":"10.13039\/501100003130","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100003130","name":"Fonds Wetenschappelijk Onderzoek","doi-asserted-by":"publisher","award":["1830517N"],"award-info":[{"award-number":["1830517N"]}],"id":[{"id":"10.13039\/501100003130","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100004497","name":"Onderzoeksraad, KU Leuven","doi-asserted-by":"publisher","award":["EZX\u2010C9725\u2010METH\/14\/05"],"award-info":[{"award-number":["EZX\u2010C9725\u2010METH\/14\/05"]}],"id":[{"id":"10.13039\/501100004497","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Neurogastroenterology Motil"],"published-print":{"date-parts":[[2026,1]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Disorders of gut\u2010brain interaction (DGBI), such as functional dyspepsia and irritable bowel syndrome, are characterized by immune activation and increased permeability in the gastrointestinal tract. However, their role in symptom generation remains unclear. Using the normoglycemic Biobreeding diabetes\u2010prone rat (BBDP\u2010N) as a spontaneous model of DGBI, we aim to (1) further characterize the inflammatory infiltrate in the intestinal mucosa and (2) elucidate the relationship between immune activation, barrier function, and colonic sensitivity by studying the effect of a local anti\u2010inflammatory corticosteroid treatment, budesonide.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Ninety\u2010day\u2010old BBDP\u2010N and control rats were treated with budesonide (0.5\u2009mg\/kg\/day) or vehicle for 28\u2009days. Jejunal and colonic eosinophil and mast cell numbers and activation were assessed, as well as permeability and colonic sensitivity.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Key Results<\/jats:title>\n                    <jats:p>Eosinophil and mast cell numbers, as well as eosinophil but not mast cell activation were increased in BBDP\u2010N rats. After budesonide treatment, eosinophil and mast cell infiltration decreased. Colonic sensitivity increased over time in BBDP\u2010N rats, which was prevented when treated with budesonide, and a limited effect on permeability in budesonide\u2010treated BBDP\u2010N rats was also observed after treatment.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Together, these results demonstrate that a local anti\u2010inflammatory treatment improved intestinal permeability and visceral hypersensitivity in a preclinical, spontaneous model of DGBI. Moreover, it supports a role for intestinal inflammation in the intestinal barrier defect and symptoms, further paving the way for additional evaluation of anti\u2010inflammatory treatments, including budesonide, in DGBI.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/nmo.70233","type":"journal-article","created":{"date-parts":[[2026,1,28]],"date-time":"2026-01-28T14:42:47Z","timestamp":1769611367000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Oral Local Budesonide Treatment Ameliorates Immune Activation and Colonic Sensitivity in a Spontaneous Model for Disorders of Gut\u2010Brain Interaction"],"prefix":"10.1111","volume":"38","author":[{"given":"Alison","family":"Accarie","sequence":"first","affiliation":[{"name":"Translational Research Center for Gastrointestinal Disorders (TARGID) University of Leuven  Leuven 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