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Gut barrier dysfunction : a primary defect in twins with Crohn's disease predominantly caused by genetic predisposition
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- Keita, Åsa (författare)
- Linköpings universitet,Avdelningen för Kirurgi, Ortopedi och Onkologi,Medicinska fakulteten
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- Lindqvist, Carl Mårten, 1979- (författare)
- Örebro universitet,Institutionen för medicinska vetenskaper,Department of Medical Sciences,Örebro University, Örebro, Sweden
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- Öst, Åke (författare)
- Department of Pathology and Cytology, Aleris Medilab, Täby, Sweden
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- (creator_code:org_t)
- 2018-04-12
- 2018
- Engelska.
- Ingår i: Journal of Crohn's & Colitis. - : Elsevier. - 1873-9946 .- 1876-4479. ; 12:10, s. 1200-1209
- Tidskriftsartikel (refereegranskat)
Abstract
Ämnesord
Stäng
- 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.
Ämnesord
- MEDICIN OCH HÄLSOVETENSKAP -- Klinisk medicin -- Gastroenterologi (hsv//swe)
- MEDICAL AND HEALTH SCIENCES -- Clinical Medicine -- Gastroenterology and Hepatology (hsv//eng)
Nyckelord
- Crohn's disease
- barrier function
- genetics
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- ref (ämneskategori)
- art (ämneskategori)
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- Keita, Åsa
- Lindqvist, Carl ...
- Öst, Åke
- Ley Magana, Carl ...
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- Halfvarson, Jona ...
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