ArticleInternational journal of molecular sciences2021
Yersiniabactin Siderophore of Crohn's Disease-Associated Adherent-Invasive
Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 15 citations in OpenAlex.
- Whole-genome analysis of fiveMicrobiology spectrum · 2025Article
- Yersiniabactin produced byFrontiers in microbiology · 2025Article
- Autophagy and Bacterial infections.Autophagy reports · 2025Review
- ATG16L1 in myeloid cells limits colorectal tumor growth inAutophagy · 2024Article
- Siderophore-harboring gut bacteria and fecal siderophore genes for predicting the responsiveness of fecal microbiota transplantation for active ulcerative colitis.Journal of translational medicine · 2024Article
- Article
- Identification of autophagy receptors for the Crohn's disease-associated adherent-invasiveFrontiers in cellular and infection microbiology · 2024Article
- Yersiniabactin-ProducingInternational journal of molecular sciences · 2023Article
- Molecular analysis of clinicalFrontiers in microbiology · 2023Article
- Role of adherent invasiveWorld journal of clinical cases · 2022Review
- Genomics and pathotypes of the many faces of Escherichia coli.FEMS microbiology reviews · 2022Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
backgroundAdherent-invasive
methodsIntestinal epithelial T84 cells and CEABAC10 transgenic mice were infected with LF82 or its mutants deficient in yersiniabactin expression. Autophagy was assessed by Western blot analysis for p62 and LC3-II expression.
resultsLoss of yersiniabactin decreased the growth of LF82 in competitive conditions, reducing the ability of LF82 to adhere to and invade T84 cells and to colonize the intestinal tract of CEABAC10 mice. However, yersiniabactin deficiency increased LF82 intracellular replication. Mechanistically, a functional yersiniabactin is necessary for LF82-induced expression of HIF-1α, which is implicated in autophagy activation in infected cells.
conclusionOur study highlights a novel role for yersiniabactin siderophore in AIEC-host interaction. Indeed, yersiniabactin, which is an advantage for AIEC to growth in a competitive environment, could be a disadvantage for the bacteria as it activates autophagy, a key host defense mechanism, leading to bacterial clearance.
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Registered trials
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