{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,3]],"date-time":"2026-11-03T21:06:44Z","timestamp":1793740004117,"version":"4.6.1"},"reference-count":30,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"8","license":[{"start":{"date-parts":[[2019,8,1]],"date-time":"2019-08-01T00:00:00Z","timestamp":1564617600000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Clin Transl Gastroenterol","Clinical and Translational Gastroenterology"],"abstract":"<jats:sec>\n                    <jats:title>OBJECTIVES:<\/jats:title>\n                    <jats:p>Chronic liver disease (CLD) is associated with both alterations of the stool microbiota and increased small intestinal permeability. However, little is known about the role of the small intestinal mucosa-associated microbiota (MAM) in CLD. The aim of this study was to evaluate the relationship between the duodenal MAM and both small intestinal permeability and liver disease severity in CLD.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>METHODS:<\/jats:title>\n                    <jats:p>Subjects with CLD and a disease-free control group undergoing routine endoscopy underwent duodenal biopsy to assess duodenal MAM by 16S rRNA gene sequencing. Small intestinal permeability was assessed by a dual sugar (lactulose: rhamnose) assay. Other assessments included transient elastography, endotoxemia, serum markers of hepatic inflammation, dietary intake, and anthropometric measurements.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>RESULTS:<\/jats:title>\n                    <jats:p>\n                      Forty-six subjects (35 with CLD and 11 controls) were assessed. In subjects with CLD, the composition (\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      = 0.02) and diversity (\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      &lt; 0.01) of the duodenal MAM differed to controls. Constrained multivariate analysis and linear discriminate effect size showed this was due to Streptococcus-affiliated lineages. Small intestinal permeability was significantly higher in CLD subjects compared to controls. In CLD, there were inverse correlations between microbial diversity and both increased small intestinal permeability (\n                      <jats:italic toggle=\"yes\">r<\/jats:italic>\n                      = \u22120.41,\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      = 0.02) and serum alanine aminotransferase (\n                      <jats:italic toggle=\"yes\">r<\/jats:italic>\n                      = \u22120.35,\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      = 0.04). Hepatic stiffness was not associated with the MAM.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>DISCUSSION:<\/jats:title>\n                    <jats:p>In CLD, there is dysbiosis of the duodenal MAM and an inverse correlation between microbial diversity and small intestinal permeability.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>TRANSLATIONAL IMPACT:<\/jats:title>\n                    <jats:p>Strategies to ameliorate duodenal MAM dysbiosis may ameliorate intestinal barrier dysfunction and liver injury in CLD.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.14309\/ctg.0000000000000068","type":"journal-article","created":{"date-parts":[[2019,8,2]],"date-time":"2019-08-02T12:35:18Z","timestamp":1564749318000},"page":"e00068","source":"Crossref","is-referenced-by-count":25,"title":["Dysbiosis of the Duodenal Mucosal Microbiota Is Associated With Increased Small Intestinal Permeability in Chronic Liver Disease"],"prefix":"10.14309","volume":"10","author":[{"given":"Ashok S.","family":"Raj","sequence":"first","affiliation":[{"name":"Department of Gastroenterology and Hepatology, Princess Alexandra Hospital, Woolloongabba, Queensland, Australia;"},{"name":"School of Medicine, Faculty of Medicine and Biomedical Sciences, the University of Queensland, and Translational Research Institute, Woolloongabba, Queensland, Australia;"},{"name":"School of Medicine, the University of Auckland, Auckland, New Zealand;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Erin R.","family":"Shanahan","sequence":"additional","affiliation":[{"name":"Department of Gastroenterology and Hepatology, Princess Alexandra Hospital, Woolloongabba, Queensland, Australia;"},{"name":"School of Medicine, Faculty of Medicine and Biomedical Sciences, the University of Queensland, and Translational Research Institute, Woolloongabba, Queensland, Australia;"},{"name":"Microbial Biology and Metagenomics Research Group, the University of Queensland Diamantina Institute, Translational Research Institute, Woolloongabba, Queensland, Australia;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Cuong D.","family":"Tran","sequence":"additional","affiliation":[{"name":"Health and Biosecurity, Commonwealth Scientific and Industrial Research Organisation (CSIRO), Adelaide, South Australia, Australia;"},{"name":"School of Medicine, Faculty of Health Sciences, University of Adelaide, Adelaide, South Australia, Australia;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Purnima","family":"Bhat","sequence":"additional","affiliation":[{"name":"Australian National University School of Medicine, Australian National University, Canberra, Australia."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Linda M.","family":"Fletcher","sequence":"additional","affiliation":[{"name":"Department of Gastroenterology and Hepatology, Princess Alexandra Hospital, Woolloongabba, Queensland, Australia;"},{"name":"School of Medicine, Faculty of Medicine and Biomedical Sciences, the University of Queensland, and Translational Research Institute, Woolloongabba, Queensland, Australia;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David A.","family":"Vesey","sequence":"additional","affiliation":[{"name":"School of Medicine, Faculty of Medicine and Biomedical Sciences, the University of Queensland, and Translational Research Institute, Woolloongabba, Queensland, Australia;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mark","family":"Morrison","sequence":"additional","affiliation":[{"name":"Microbial Biology and Metagenomics Research Group, the University of Queensland Diamantina Institute, Translational Research Institute, Woolloongabba, Queensland, 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