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Enhanced E. coli LF82 Translocation through the Follicle-associated Epithelium in Crohns Disease is Dependent on Long Polar Fimbriae and CEACAM6 expression, and Increases Paracellular Permeability
Linköpings universitet, Institutionen för biomedicinska och kliniska vetenskaper, Avdelningen för kirurgi, ortopedi och onkologi. Linköpings universitet, Medicinska fakulteten.ORCID-id: 0000-0002-6820-0215
Linköpings universitet, Institutionen för biomedicinska och kliniska vetenskaper, Avdelningen för kirurgi, ortopedi och onkologi. Linköpings universitet, Medicinska fakulteten.
Linköpings universitet, Institutionen för biomedicinska och kliniska vetenskaper, Avdelningen för kirurgi, ortopedi och onkologi. Linköpings universitet, Medicinska fakulteten.
Linköpings universitet, Institutionen för biomedicinska och kliniska vetenskaper, Avdelningen för molekylär medicin och virologi. Linköpings universitet, Medicinska fakulteten.ORCID-id: 0000-0001-8817-6403
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2020 (engelsk)Inngår i: Journal of Crohn's & Colitis, ISSN 1873-9946, E-ISSN 1876-4479, Vol. 14, nr 2, s. 216-229Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Background and Aims: Patients with Crohns disease [CD] harbour an increased number of adherent-invasive E. coli [AIEC]. The strain LF82, identified in the ileal mucosa of CD patients, has been extensively studied for pathogenic mechanisms. However, understanding of the interaction of LF82 with the intestinal mucosa of CD patients is lacking. Methods: Here, we investigated the importance of long polar fimbriae [LPF] type 1 pili and the carcinoembryonic antigen-related cell-adhesion molecule 6 [CEACAM6] for translocation of LF82 in an in vitro model of follicle-associated epithelium [FAE], and in the FAE and villus epithelium [VE] of patients with CD and controls, using Ussing chambers. Results: Significantly greater LF82 passage occurred in the FAE model compared with in the VE Caco-2cl1 mono-culture. Moreover, bacterial translocation was inhibited by either LPF disruption or pre-incubation with anti-CEACAM6 antibody. Tissue mounted in Ussing chambers showed significantly higher LF82 passage in FAE from patients with CD compared with control FAE, that was diminished in LF82 lacking LPF and by blocking host CEACAM6. Interestingly, addition of LF82 to the CD FAE tissues significantly increased paracellular permeability [of (51)Chromium-EDTA] compared with baseline, and the increase was inhibited by anti-CEACAM6. Immunofluorescence and immunoblots showed higher expression of CEACAM6 in FAE of patients with CD compared with in FAE from controls. Conclusions: These data suggest that the FAE of CD patients is a site of vulnerability for invasion by LF82 via a mechanism that requires both bacterial LPF and host CEACAM6. Further, LF82 has the ability to increase paracellular passage through the FAE of patients with CD. These data can help define novel therapeutic targets in CD for the prevention of clinical recurrence.

sted, utgiver, år, opplag, sider
OXFORD UNIV PRESS , 2020. Vol. 14, nr 2, s. 216-229
Emneord [en]
Inflammatory bowel disease; mucosal barrier; permeability
HSV kategori
Identifikatorer
URN: urn:nbn:se:liu:diva-164394DOI: 10.1093/ecco-jcc/jjz144ISI: 000515116000009PubMedID: 31393983OAI: oai:DiVA.org:liu-164394DiVA, id: diva2:1415846
Merknad

Funding Agencies|International Organization for the Study of Inflammatory Bowel Disease; Lions Clubs International Foundation; Swedish Research Council [VR-Medicine and Health] [2014-02537, 2017-02475]; ALF Grants Region Ostergotland

Tilgjengelig fra: 2020-03-20 Laget: 2020-03-20 Sist oppdatert: 2020-04-15

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Keita, ÅsaYakimenko Alkaissi, LinaBoström Holm, ElinHeil, StéphanieSöderholm, Johan D
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