Yersinia enterocolitica YopT and Clostridium difficile toxin B induce expression of GILZ in epithelial cells
Autor: | Bernhard Lüscher, Marie Liesse Asselin-Labat, Martin Köberle, Simon Langer, Erwin Bohn, Robert Zumbihl, David Göppel, Ingo B. Autenrieth, Tanja Grandl, Peer Gaentzsch, Steffen Müller, Susanne Berchtold, Birgit Manncke, Holger Barth, Marc Pallardy, Isabel Sorg |
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Přispěvatelé: | Eberhard Karls Universität Tübingen = Eberhard Karls University of Tuebingen, RWTH Aachen University, Université Paris-Sud - Paris 11 (UP11), The Walter and Eliza Hall Institute of Medical Research (WEHI), Biozentrum [Basel, Suisse], University of Basel (Unibas), Universität Ulm - Ulm University [Ulm, Allemagne], Diversité, Génomes et Interactions Microorganismes-Insectes, Institut National de la Recherche Agronomique (INRA)-Université Montpellier 2 - Sciences et Techniques (UM2), Université Montpellier 2 - Sciences et Techniques (UM2), Deutsche Forschungsgemeinschaft |
Jazyk: | angličtina |
Rok vydání: | 2012 |
Předmět: |
rho GTP-Binding Proteins
Bacterial Diseases RHOA Transcription Genetic RHOB [SDV]Life Sciences [q-bio] NF-KAPPA-B Gene Expression lcsh:Medicine Apoptosis GTPase Toxicology E-Box Elements Molecular cell biology PROTECTS T-LYMPHOCYTES Gene expression Promoter Regions Genetic lcsh:Science 0303 health sciences GENE-PRODUCT RHOB Multidisciplinary Protein translation biology Mechanisms of Signal Transduction BINDING PROTEINS NF-kappa B 3. Good health Cysteine Endopeptidases Infectious Diseases VIRULENCE PLASMID Medicine INDUCED LEUCINE-ZIPPER SIGNALING PATHWAY Inflammation Mediators Mitogen-Activated Protein Kinases Signal transduction Signal Transduction Research Article Transcriptional Activation Clostridium Difficile Bacterial Toxins DNA transcription Toxic Agents Clostridium difficile toxin B THYMOCYTE APOPTOSIS Microbiology Yersiniosis DENDRITIC CELLS 03 medical and health sciences Bacterial Proteins Downregulation and upregulation Virology Humans Biology Transcription factor 030304 developmental biology Inflammation Base Sequence 030306 microbiology Gene Expression Profiling lcsh:R Epithelial Cells INVASIN PROTEIN Molecular biology Virulence Factors and Mechanisms biology.protein Upstream Stimulatory Factors lcsh:Q HeLa Cells Transcription Factors |
Zdroj: | Plos One 7 (7), . (2012) PLoS ONE PLoS ONE, Public Library of Science, 2012, 7 (7), ⟨10.1371/journal.pone.0040730⟩ PLoS ONE, Vol 7, Iss 7, p e40730 (2012) PLOS ONE 7(7), e40730 (2012). doi:10.1371/journal.pone.0040730 |
ISSN: | 1932-6203 |
DOI: | 10.1371/journal.pone.0040730⟩ |
Popis: | International audience; Glucocorticoid induced-leucine zipper (GILZ) has been shown to be induced in cells by different stimuli such as glucocorticoids, IL-10 or deprivation of IL-2. GILZ has anti-inflammatory properties and may be involved in signalling modulating apoptosis. Herein we demonstrate that wildtype Yersinia enterocolitica which carry the pYV plasmid upregulated GILZ mRNA levels and protein expression in epithelial cells. Infection of HeLa cells with different Yersinia mutant strains revealed that the protease activity of YopT, which cleaves the membrane-bound form of Rho GTPases was sufficient to induce GILZ expression. Similarly, Clostridium difficile toxin B, another bacterial inhibitor of Rho GTPases induced GILZ expression. YopT and toxin B both increased transcriptional activity of the GILZ promoter in HeLa cells. GILZ expression could not be linked to the inactivation of an individual Rho GTPase by these toxins. However, forced expression of RhoA and RhoB decreased basal GILZ promoter activity. Furthermore, MAPK activation proved necessary for profound GILZ induction by toxin B. Promoter studies and gel shift analyses defined binding of upstream stimulatory factor (USF) 1 and 2 to a canonical c-Myc binding site (E-box) in the GILZ promoter as a crucial step of its trans-activation. In addition we could show that USF-1 and USF-2 are essential for basal as well as toxin B induced GILZ expression. These findings define a novel way of GILZ promoter trans-activation mediated by bacterial toxins and differentiate it from those mediated by dexamethasone or deprivation of IL-2. |
Databáze: | OpenAIRE |
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