Yersiniabactin siderophore of Crohn’s disease-associated adherent-invasive Escherichia coli Is Involved in autophagy activation in host cells
| Autor: | Nicolas Barnich, Sébastien Massier, Richard Bonnet, Emilie Vazeille, Guillaume Dalmasso, Hang Thi Thu Nguyen, Tiphanie Faïs, Julien Delmas, Caroline Chevarin |
|---|---|
| Přispěvatelé: | Microbes, Intestin, Inflammation et Susceptibilité de l'Hôte (M2iSH), Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre de Recherche en Nutrition Humaine d'Auvergne (CRNH d'Auvergne)-Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE)-Université Clermont Auvergne (UCA), Centre de Recherche en Nutrition Humaine Auvergne [CHU Clermont-Ferrand] (CRNH A), Direction de la recherche clinique et de l’innovation [CHU Clermont-Ferrand] (DRCI), CHU Clermont-Ferrand-CHU Clermont-Ferrand, Service de Bactériologie [CHU Clermont-Ferrand], CHU Gabriel Montpied [Clermont-Ferrand], Service d'Hépatologie Gastro-entérologie [CHU Clermont-Ferrand], CHU Estaing [Clermont-Ferrand], Infection Inflammation et Interaction Hôtes Pathogènes [CHU Clermont-Ferrand] (3IHP ), Centre National de Référence de la Résistance aux Antibiotiques [CHU Clermont-Ferrand] (CNR), CHU Clermont-Ferrand, Ministere de la Recherche et de la Technologie, Inserm, INRAE, Association Francois Aupetit, ANR-16-IDEX-0001,CAP 20-25,CAP 20-25(2016), European Project: 12420,FP7-PEOPLE-IIF-2008 |
| Jazyk: | angličtina |
| Rok vydání: | 2021 |
| Předmět: |
0301 basic medicine
Crohn’s disease Siderophore autophagy siderophore Mutant Yersinia medicine.disease_cause Yersiniabactin Catalysis Microbiology lcsh:Chemistry Inorganic Chemistry 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine MESH: Phenols/metabolism medicine Physical and Theoretical Chemistry lcsh:QH301-705.5 Molecular Biology Escherichia coli Spectroscopy MESH: Escherichia coli Infections/Complications MESH: Escherichia coli/pathogenicity biology Organic Chemistry Autophagy HIF-1alpha MESH: autophagy MESH: intestinal mucosa/physiopathology [SDV.MHEP.HEG]Life Sciences [q-bio]/Human health and pathology/Hépatology and Gastroenterology General Medicine MESH: Thiazoles/metabolism MESH: Crohn Disease/etiology biology.organism_classification Pathogenicity island Computer Science Applications 030104 developmental biology lcsh:Biology (General) lcsh:QD1-999 chemistry 030211 gastroenterology & hepatology Bacteria AIEC |
| Zdroj: | International Journal of Molecular Sciences International Journal of Molecular Sciences, 2021, 22 (7), pp.1-17. ⟨10.3390/ijms22073512⟩ Volume 22 Issue 7 International Journal of Molecular Sciences, MDPI, 2021, 22 (7), pp.1-17. ⟨10.3390/ijms22073512⟩ International Journal of Molecular Sciences, Vol 22, Iss 3512, p 3512 (2021) |
| ISSN: | 1661-6596 1422-0067 |
| Popis: | International audience; Background: Adherent-invasive Escherichia coli (AIEC) have been implicated in the etiology of Crohn’s disease. The AIEC reference strain LF82 possesses a pathogenicity island similar to the high pathogenicity island of Yersinia spp., which encodes the yersiniabactin siderophore required for iron uptake and growth of the bacteria in iron-restricted environment. Here, we investigated the role of yersiniabactin during AIEC infection. Methods: Intestinal 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. Results: Loss 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. Conclusion: Our 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. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|