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2021 (English) In: Scandinavian Journal of Gastroenterology, ISSN 0036-5521, E-ISSN 1502-7708, Vol. 56, no 11, p. 1286-1295Article in journal (Refereed) Published
Abstract [en] BACKGROUND: Environmental factors are strongly implicated in late-onset of inflammatory bowel disease. Here, we investigate whether high levels of perfluoroalkyl substances are associated with (1) late-onset inflammatory bowel disease, and (2) disturbances of the bile acid pool. We further explore the effect of the specific perfluoroalkyl substance perfluorooctanoic acid on intestinal barrier function in murine tissue.
METHODS: Serum levels of perfluoroalkyl substances and bile acids were assessed by ultra-performance liquid chromatography coupled to a triple-quadrupole mass spectrometer in matched samples from patients with ulcerative colitis (n = 20) and Crohn's disease (n = 20) diagnosed at the age of ≥55 years. Age and sex-matched blood donors (n = 20), were used as healthy controls. Ex vivo Ussing chamber experiments were performed to assess the effect of perfluorooctanoic acid on ileal and colonic murine tissue (n = 9).
RESULTS: The total amount of perfluoroalkyl substances was significantly increased in patients with ulcerative colitis compared to healthy controls and patients with Crohn's disease (p < .05). Ex vivo exposure to perfluorooctanoic acid induced a significantly altered ileal and colonic barrier function. The distribution of bile acids, as well as the correlation pattern between (1) perfluoroalkyl substances and (2) bile acids, differed between patient and control groups.
DISCUSSION: Our results demonstrate that perfluoroalkyl substances levels are increased in patients with late-onset ulcerative colitis and may contribute to the disease by inducing a dysfunctional intestinal barrier.
Place, publisher, year, edition, pages
Taylor & Francis, 2021
Keywords PFAS, bile acids, inflammatory bowel disease, intestinal barrier function, ulcerative colitis
National Category
Gastroenterology and Hepatology
Identifiers urn:nbn:se:oru:diva-93618 (URN) 10.1080/00365521.2021.1961306 (DOI) 000684451500001 () 34383611 (PubMedID) 2-s2.0-85112297285 (Scopus ID)
Funder Swedish Research Council, 2016-05176European CommissionSwedish Research Council Formas, 2019-00869
Note Funding Agencies:
Faculty of Medicine and Health, Örebro University ORU2018/04457
Bo Rydin foundation F0514
Örebro Hospital Research Foundation OLL-790011
2021-08-162021-08-162025-02-11 Bibliographically approved