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Gut barrier dysfunc...
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Keita, ÅsaLinköpings universitet,Avdelningen för Kirurgi, Ortopedi och Onkologi,Medicinska fakulteten
(author)
Gut barrier dysfunction : a primary defect in twins with Crohn's disease predominantly caused by genetic predisposition
- Article/chapterEnglish2018
Publisher, publication year, extent ...
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2018-04-12
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Elsevier,2018
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printrdacarrier
Numbers
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LIBRIS-ID:oai:DiVA.org:oru-66791
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https://urn.kb.se/resolve?urn=urn:nbn:se:oru:diva-66791URI
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https://doi.org/10.1093/ecco-jcc/jjy045DOI
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https://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-154129URI
Supplementary language notes
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Language:English
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Summary in:English
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Subject category:ref swepub-contenttype
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Subject category:art swepub-publicationtype
Notes
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Funding Agency:Region Östergötland, ALF research funds of Linköping University
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Funding Agencies|Swedish Research Council-Medicine [VR-MH 2014-02537, 521-2011-2764]; Region Ostergotland, ALF research funds of Linkoping University
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Background and aims: The aetiology of Crohn's disease is poorly understood. By investigating twin pairs discordant for Crohn's disease we aimed to assess if the dysregulated barrier represents a cause or a consequence of inflammation and to evaluate the impact of genetic predisposition on barrier function.Methods: Ileal biopsies from 15 twin pairs discordant for Crohn's disease (monozygotic n=9, dizygotic n=6) and 10 external controls were mounted in Ussing chambers to assess paracellular permeability to51Chromium (Cr)-EDTA and trancellular passage to non-pathogenic E. coli K-12. Experiments were performed with and without provocation with acetylsalicylic acid. Immunofluorescence and ELISA were used to quantify the expression level of tight junction proteins.Results: Healthy co-twins and affected twins displayed increased 51Cr-EDTA permeability at 120 min both with Acetylsalicylic acid (p<0.001) and without (p<0.001) when compared to controls. A significant increase in 51Cr-EDTA flux was seen already at 20 minutes in healthy monozygotic co-twins compared to controls (p≤0.05) when stratified by zygosity, but not in healthy dizygotic co-twins. No difference in E. coli passage was observed between groups. Immunofluorescence of the tight junction proteins claudin-5 and tricellulin showed lower levels in healthy co-twins (p<0.05) and affected twins (p<0.05) compared to external controls, while ELISA only showed lower tricellulin in Crohn's disease twins (p<0.05).Conclusion: Our results suggest that barrier dysfunction is a primary defect in Crohn's disease, since changes were predominantly seen in healthy monozygotic co-twins. Passage of E. coli seems to be a consequence of inflammation rather than representing a primary defect.
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Lindqvist, Carl Mårten,1979-Örebro universitet,Institutionen för medicinska vetenskaper,Department of Medical Sciences,Örebro University, Örebro, Sweden(Swepub:oru)melt
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Öst, ÅkeDepartment of Pathology and Cytology, Aleris Medilab, Täby, Sweden
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Ley Magana, Carlos DanielLinköpings universitet,Avdelningen för kliniska vetenskaper,Medicinska fakulteten(Swepub:liu)carle20
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Schoultz, Ida,1979-Örebro universitet,Institutionen för medicinska vetenskaper,Department of Medical Sciences,Örebro University, Örebro, Sweden(Swepub:oru)isz
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Halfvarson, Jonas,1970-Örebro universitet,Institutionen för medicinska vetenskaper,Department of Gastroenterology,Örebro University, Örebro, Sweden(Swepub:oru)jshn
(author)
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Linköpings universitetAvdelningen för Kirurgi, Ortopedi och Onkologi
(creator_code:org_t)
Related titles
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In:Journal of Crohn's & Colitis: Elsevier12:10, s. 1200-12091873-99461876-4479
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