ArticleGut pathogens2021
Adherent invasive Escherichia coli (AIEC) strain LF82, but not Candida albicans, plays a profibrogenic role in the intestine.
Article in Gut pathogens, 2021. 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, 15 citations in OpenAlex.
- Gut Microbiota as a Mediator Between Intestinal Fibrosis and Creeping Fat in Crohn's Disease.United European gastroenterology journal · 2025Review
- ECM formation and degradation during fibrosis, repair, and regeneration.npj metabolic health and disease · 2025Review
- Inflammation-fibrosis interplay in inflammatory bowel disease: mechanisms, progression, and therapeutic strategies.Frontiers in pharmacology · 2025Review
- Preventing fibrosis in IBD: update on immune pathways and clinical strategies.Expert review of clinical immunology · 2024Review
- Macrophage polarization: an important role in inflammatory diseases.Frontiers in immunology · 2024Review
- Role of adherent invasiveWorld journal of clinical cases · 2022Review
- Revisiting fibrosis in inflammatory bowel disease: the gut thickens.Nature reviews. Gastroenterology & hepatology · 2022Review
- Intestinal strictures in Crohn's disease: a 2021 update.Therapeutic advances in gastroenterology · 2022Review
- Adherent-Invasive and Non-InvasiveMicroorganisms · 2021Article
- Article
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Authors and funding
8 authors at 2 institutions in 1 country.
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Abstract
backgroundIntestinal fibrosis is a frequent complication of Crohn's disease. However, the factors that cause chronicity and promote fibrogenesis are not yet understood.
aimsIn the present study, we evaluated the profibrotic effects of adherent-invasive Escherichia coli (AIEC) LF82 strain and Candida albicans in the gut.
methodsColonic fibrosis was induced in C57BL/6 mice by administration of three cycles of 2.5% (w/v) dextran sulfate sodium (DSS) for 5 weeks. LF82 and C. albicans were administered orally once at the start of each week or each cycle, respectively. Expression of markers of myofibroblast activation was determined in TGF-β1-stimulated human intestinal epithelial cells (IECs).
resultsLF82 administration exacerbated fibrosis in DSS-treated mice, revealed by increased colonic collagen deposition and expression of the profibrotic genes Col1a1, Col3a1, Fn1 and Vim. This was accompanied by enhanced gene expression of proinflammatory cytokines and chemokines, as well as more recruited inflammatory cells into the intestine. LF82 also potentiated TGF-β1-stimulated epithelial-mesenchymal transition and myofibroblast activation in IECs, by further inducing gene expression of the main mesenchymal cell markers FN1 and VIM and downregulating the IEC marker OCLN. Proinflammatory cytokines were overexpressed with LF82 in TGF-β1-stimulated IECs. Conversely, C. albicans did not affect intestinal fibrosis progression in DSS-treated mice or myofibroblast activation in TGF-β1-stimulated IECs.
conclusionsThese results demonstrate that AIEC strain LF82, but not C. albicans, may play a major profibrogenic role in the gut.
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