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While possible triggers have been identified, research is inconsistent on the precise cause of these relapses, especially in the under-researched pediatric population. We hypothesized that patients in remission would have persistent microbial and inflammatory changes in small intestinal tissue that might trigger relapse. To this end, we analyzed intestinal biopsy samples from six patients with pediatric Crohn\u2019s disease in remission and a control group of 16 pediatric patients with no evident pathogenic abnormality. We identified compositional microbiota differences, including decreases in the genera <jats:italic>Streptococcus<\/jats:italic> and <jats:italic>Actinobacillus<\/jats:italic> as well as increases in <jats:italic>Oribacterium<\/jats:italic> and <jats:italic>Prevotella<\/jats:italic> in patients with controlled Crohn\u2019s disease compared to controls. Further, a histologic analysis found that patients with controlled Crohn\u2019s disease had increased epithelial integrity, and decreased intraepithelial lymphocytes compared with controls. Additionally, we observed increased peripheral CD4<jats:sup>+<\/jats:sup> T cells in patients with pediatric Crohn\u2019s disease. These results indicate that markers of intestinal inflammation are responsive to Crohn\u2019s disease treatment, however the interventions may not resolve the underlying dysbiosis. These findings suggest that persistent dysbiosis may increase vulnerability to relapse of pediatric Crohn\u2019s disease. This study used a nested cohort of patients from the Bangladesh Environmental Enteric Dysfunction (BEED) study (ClinicalTrials.gov ID: NCT02812615 Date of first registration: 24\/06\/2016).<\/jats:p>","DOI":"10.1038\/s41598-024-63299-y","type":"journal-article","created":{"date-parts":[[2024,6,3]],"date-time":"2024-06-03T06:02:32Z","timestamp":1717394552000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":11,"title":["Persistent dysbiosis of duodenal microbiota in patients with controlled pediatric Crohn\u2019s disease after resolution of inflammation"],"prefix":"10.1038","volume":"14","author":[{"given":"Rebecca","family":"Pierce","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ning-Jiun","family":"Jan","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pankaj","family":"Kumar","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jeremy","family":"Middleton","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7268-1218","authenticated-orcid":false,"given":"William A.","family":"Petri","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chelsea","family":"Marie","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2024,6,3]]},"reference":[{"key":"63299_CR1","doi-asserted-by":"publisher","first-page":"373","DOI":"10.1016\/j.bpg.2014.04.009","volume":"28","author":"JZ Liu","year":"2014","unstructured":"Liu, J. 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