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
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