Hypoxia Decreases Invasin-Mediated Yersinia enterocolitica Internalization into Caco-2 Cells.
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AbstractYersinia enterocolitica is a major cause of human yersiniosis, with enterocolitis being a typical manifestation. These bacteria can cross the intestinal mucosa, and invade eukaryotic cells by binding to host β1 integrins, a process mediated by the bacterial effector protein invasin. This study examines the role of hypoxia on the internalization of Y. enterocolitica into intestinal epithelial cells, since the gastrointestinal tract has been shown to be physiologically deficient in oxygen levels (hypoxic), especially in cases of infection and inflammation. We show that hypoxic pre-incubation of Caco-2 cells resulted in significantly decreased bacterial internalization compared to cells grown under normoxia. This phenotype was absent after functionally blocking host β1 integrins as well as upon infection with an invasin-deficient Y. enterocolitica strain. Furthermore, downstream phosphorylation of the focal adhesion kinase was also reduced under hypoxia after infection. In good correlation to these data, cells grown under hypoxia showed decreased protein levels of β1 integrins at the apical cell surface whereas the total protein level of the hypoxia inducible factor (HIF-1) alpha was elevated. Furthermore, treatment of cells with the HIF-1 α stabilizer dimethyloxalylglycine (DMOG) also reduced invasion and decreased β1 integrin protein levels compared to control cells, indicating a potential role for HIF-1α in this process. These results suggest that hypoxia decreases invasin-integrin-mediated internalization of Y. enterocolitica into intestinal epithelial cells by reducing cell surface localization of host β1 integrins.
CitationHypoxia Decreases Invasin-Mediated Yersinia enterocolitica Internalization into Caco-2 Cells. 2016, 11 (1):e0146103 PLoS ONE
AffiliationHelmholtz Centre for infection research, Inhoffenstr. 7, D-38124 Braunschweig, Germany.
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- Translocation of Yersinia entrocolitica across reconstituted intestinal epithelial monolayers is triggered by Yersinia invasin binding to beta1 integrins apically expressed on M-like cells.
- Authors: Schulte R, Kerneis S, Klinke S, Bartels H, Preger S, Kraehenbuhl JP, Pringault E, Autenrieth IB
- Issue date: 2000 Apr
- Expression and distribution of beta1 integrins in in vitro-induced M cells: implications for Yersinia adhesion to Peyer's patch epithelium.
- Authors: Hamzaoui N, Kernéis S, Caliot E, Pringault E
- Issue date: 2004 Sep
- Yersinia enterocolitica exploits different pathways to accomplish adhesion and toxin injection into host cells.
- Authors: Keller B, Mühlenkamp M, Deuschle E, Siegfried A, Mössner S, Schade J, Griesinger T, Katava N, Braunsdorf C, Fehrenbacher B, Jiménez-Soto LF, Schaller M, Haas R, Genth H, Retta SF, Meyer H, Böttcher RT, Zent R, Schütz M, Autenrieth IB, Bohn E
- Issue date: 2015 Aug
- Neisseria meningitidis adhesin NadA targets beta1 integrins: functional similarity to Yersinia invasin.
- Authors: Nägele V, Heesemann J, Schielke S, Jiménez-Soto LF, Kurzai O, Ackermann N
- Issue date: 2011 Jun 10
- Yersinia enterocolitica invasin triggers phagocytosis via beta1 integrins, CDC42Hs and WASp in macrophages.
- Authors: Wiedemann A, Linder S, Grassl G, Albert M, Autenrieth I, Aepfelbacher M
- Issue date: 2001 Oct