ArticleDisease models & mechanisms2022
An adherent-invasive Escherichia coli-colonized mouse model to evaluate microbiota-targeting strategies in Crohn's disease.
Article in Disease models & mechanisms, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 14 citations in OpenAlex.
- Review
- The global stress response regulatorGut microbes · 2025Article
- Supporting the evolution of infectious disease research.Disease models & mechanisms · 2024Article
- Intestinal Epithelial Creatine Transporter SLC6A8 Dysregulation in Inflammation and in Response to Adherent InvasiveInternational journal of molecular sciences · 2024Article
- Antibiotic Therapy for Active Crohn's Disease Targeting Pathogens: An Overview and Update.Antibiotics (Basel, Switzerland) · 2024Review
- Article
- Colonization of larval zebrafish (mSphere · 2023Article
- Crohn's disease: Why the ileum?World journal of gastroenterology · 2023Review
- Microbiome and Mucosal Immunity in the Intestinal Tract.In vivo (Athens, Greece)Review
- Article
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Authors and funding
7 authors at 1 institution in 1 country.
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Abstract
Adherent-invasive Escherichia coli (AIEC) were investigated for their involvement in the induction/chronicity of intestinal inflammation in Crohn's disease (CD). AIEC gut establishment is favoured by overexpression of the glycoprotein CEACAM6 in the ileal epithelium. We generated a transgenic mouse model, named 'Vill-hCC6', in which the human CEACAM6 gene was under the control of the villin promoter, conditioning expression in the small intestine. We demonstrated that CEACAM6 is strongly expressed in the small intestine mucosa and is correlated with numerous glycosylations displayed at the brush border of enterocytes. Ex vivo, the AIEC-enterocyte interaction was enhanced by CEACAM6 expression and necessitated the presence of the bacterial adhesive factor FimH. Finally, AIEC bacteria preferentially persisted in a FimH-dependent manner in the ileal mucosa of Vill-hCC6 mice compared to wild-type mice. This preclinical model opens new perspectives in the mechanistic study of the AIEC pathobiont and represents a valuable tool to evaluate the efficacy of new strategies to eliminate AIEC implanted in the ileal mucosa, such as phages, inhibitory and/or anti-virulence molecules, or CRISPR-based strategies targeting virulence or fitness factors of AIEC bacteria.
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