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17. Riboregulation in the Major Gastric Pathogen Helicobacter pylori

Author

Tejada-Arranz, Alejandro and De Reuse, Hilde

Subjects
virulence, Helicobacter pylori, small RNAs, phase variation, antisense RNAs, Review, Microbiology, post-transcriptional regulation
Abstract

Helicobacter pylori is a Gram-negative bacterial pathogen that colonizes the stomach of about half of the human population worldwide. Infection by H. pylori is generally acquired during childhood and this bacterium rapidly establishes a persistent colonization. H. pylori causes chronic gastritis that, in some cases, progresses into peptic ulcer disease or adenocarcinoma that is responsible for about 800,000 deaths in the world every year. H. pylori has evolved efficient adaptive strategies to colonize the stomach, a particularly hostile acidic environment. Few transcriptional regulators are encoded by the small H. pylori genome and post-transcriptional regulation has been proposed as a major level of control of gene expression in this pathogen. The transcriptome and transcription start sites (TSSs) of H. pylori strain 26695 have been defined at the genome level. This revealed the existence of a total of 1,907 TSSs among which more than 900 TSSs for non-coding RNAs (ncRNAs) including 60 validated small RNAs (sRNAs) and abundant anti-sense RNAs, few of which have been experimentally validated. An RNA degradosome was shown to play a central role in the control of mRNA and antisense RNA decay in H. pylori. Riboregulation, genetic regulation by RNA, has also been revealed and depends both on antisense RNAs and small RNAs. Known examples will be presented in this review. Antisense RNA regulation was reported for some virulence factors and for several type I toxin antitoxin systems, one of which controls the morphological transition of H. pylori spiral shape to round coccoids. Interestingly, the few documented cases of small RNA-based regulation suggest that their mechanisms do not follow the same rules that were well established in the model organism Escherichia coli. First, the genome of H. pylori encodes none of the two well-described RNA chaperones, Hfq and ProQ that are important for riboregulation in several organisms. Second, some of the reported small RNAs target, through “rheostat”-like mechanisms, repeat-rich stretches in the 5′-untranslated region of genes encoding important virulence factors. In conclusion, there are still many unanswered questions about the extent and underlying mechanisms of riboregulation in H. pylori but recent publications highlighted original mechanisms making this important pathogen an interesting study model.

Published
2021

22. The Helicobacter pylori GroES Cochaperonin HspA functions as a specialized nickel chaperone and sequestration protein through its unique C-terminal extension

Author

Schauer, Kristine, Muller, Cecile, Carriere, Marie, Labigne, Agnes, Cavazza, Christine, and De Reuse, Hilde

Subjects
Nickel -- Physiological aspects, Helicobacter pylori -- Physiological aspects, Molecular chaperones -- Properties, Bacterial proteins -- Properties, Biological sciences
Abstract

The transition metal nickel plays a central role in the human gastric pathogen Helicobacter pylori because it is required for two enzymes indispensable for colonization, the nickel metalloenzyme urease and [NiFe] hydrogenase. To sustain nickel availability for these metalloenzymes while providing protection from the metal's harmful effects, H. pylori is equipped with several specific nickel-binding proteins. Among these, H. pylori possesses a particular chaperone, HspA, that is a homolog of the highly conserved and essential bacterial heat shock protein GroES. HspA contains a unique His-rich C-terminal extension and was demonstrated to bind nickel in vitro. To investigate the function of this extension in H. pylori, we constructed mutants carrying either a complete deletion or point mutations in critical residues of this domain. All mutants presented a decreased intracellular nickel content measured by inductively coupled plasma mass spectrometry (ICP-MS) and reduced nickel tolerance. While urease activity was unaffected in the mutants, [NiFe] hydrogenase activity was significantly diminished when the C-terminal extension of HspA was mutated. We conclude that H. pylori HspA is involved in intracellular nickel sequestration and detoxification and plays a novel role as a specialized nickel chaperone involved in nickel-dependent maturation of hydrogenase. doi: 10.1128/JB.01216-09

Published
2010

24. Pathogenesis of Helicobacter pylori infection

Author

Denic, Milica, Touati, Eliette, De Reuse, Hilde, Pathogenèse de Helicobacter / Helicobacter Pathogenesis, Institut Pasteur [Paris]-Centre National de la Recherche Scientifique (CNRS)-Université de Paris (UP), Cellule Pasteur, Université Paris Diderot - Paris 7 (UPD7)-PRES Sorbonne Paris Cité, Our research is funded by the Institut Pasteur Transversal Research Program (PTR#73 -17), by donations of Janssen and the Odyssey Reinsurance company, by funding from the Agence Nationale de la Recherche (ANR16-CE18-0026-03, ANR15-CE17-0015) and from the 'Fondation pour la Recherche Médicale' (FRM-DBF20161136767)., We want to thank all the members of the Unité Pathogenèse de Helicobacter at the Institut Pasteur in Paris., ANR-16-CE18-0026,NADIN,BIOSYNTHESE DU NAD: VERS LA DECOUVERTE DE NOUVEAUX ANTIBACTERIENS(2016), ANR-15-CE17-0015,EMMIE,Endoscopie MultiModale pour les lésions Inflammatoires de l'Estomac(2015), and Institut Pasteur [Paris] (IP)-Centre National de la Recherche Scientifique (CNRS)-Université Paris Cité (UPCité)

Subjects
DNA methylation, cagT4SS, oncogenesis, [SDV]Life Sciences [q-bio], H pylori cell shape, VacA, chemotaxis, natural transformation, gastric organoids, miRNA
Abstract

International audience; The original strategies developed by Helicobacter pylori to persistently colonise its host and to deregulate its cellular functions make this bacterium an outstanding model to study host-pathogen interaction and the mechanisms responsible for bacterial-induced carcinogenesis. During the last year, significant results were obtained on the role of bacterial factors essential for gastric colonisation such as spiral shape maintenance, orientation through chemotaxis and the formation of bacteria clonal population islands inside the gastric glands. Particularities of the H pylori cell surface, a structure important for immune escape, were demonstrated. New insights in the bacterial stress response revealed the importance of DNA methylation-mediated regulation. Further findings were reported on H pylori components that mediate natural transformation and mechanisms of bacterial DNA horizontal transfer which maintain a high level of H pylori genetic variability. Within-host evolution was found to be niche-specific and probably associated with physiological differences between the antral and oxyntic gastric mucosa.In addition, with the progress of CryoEM, high-resolution structures of the major virulence factors, VacA and CagT4SS, were obtained. The use of gastric organoid models fostered research revealing, preferential accumulation of bacteria at the site of injury during infection. Several studies further characterised the role of CagA in the oncogenic properties of H pylori, identifying the activation of novel CagA-dependent pathways, leading to the promotion of genetic instabilities, epithelial-to-mesenchymal transition and finally carcinogenesis. Recent studies also highlight that microRNA-mediated regulation and epigenetic modifications, through DNA methylation, are key events in the H pylori-induced tumorigenesis process.

Published
2020
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25. USF1 defect drives p53 degradation during Helicobacter pylori infection and accelerates gastric carcinogenesis

Author

Costa, Lionel, Corre, Sébastien, Michel, Valérie, Le Luel, Krysten, Fernandes, Julien, Ziveri, Jason, Jouvion, Grégory, Danckaert, Anne, Mouchet, Nicolas, da Silva Barreira, David, Torres, Javier, Camorlinga, Margarita, d'Elios, Mario Milco, Fiette, Laurence, de Reuse, Hilde, Galibert, Marie-Dominique, Touati, Eliette, Pathogenèse de Helicobacter - Helicobacter Pathogenesis, Institut Pasteur [Paris] (IP)-Université Paris Diderot - Paris 7 (UPD7)-Centre National de la Recherche Scientifique (CNRS), Institut Cochin (IC UM3 (UMR 8104 / U1016)), Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Institut de Génétique et Développement de Rennes (IGDR), Université de Rennes (UR)-Centre National de la Recherche Scientifique (CNRS)-Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique ), Centre de Ressources et de Recherche Technologique - Center for Technological Resources and Research (C2RT), Institut Pasteur [Paris] (IP), Pathogénie des infections systémiques (Inserm U1002), Neuropathologie expérimentale - Experimental neuropathology, Institut Pasteur [Paris] (IP)-Université Paris Descartes - Paris 5 (UPD5), AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement, Instituto Mexicano del Seguro Social [Mexico City, Mexico] (IMSS), Università degli Studi di Firenze = University of Florence (UniFI), Institut Mutualiste de Montsouris (IMM), CHU Pontchaillou [Rennes], Université Paris Diderot, Ligue Contre le Cancer, Odyssey Reinsurance Company, FIS/IMSS/PROT/PRIO/13/027), Fondo de Investigacion en salud, IMSS, Mexico, West committee Ligue Nationale Contre le Cancer, UMS Biosit, We thank Sophie Vaulont (Institut Cochin, Paris, France) for Usf1-/- mice, Timothy C Wang (Columbia University, NY, USA) for providing us couples of INS-GAS mice and Joana Gomes and Celso Reis (I3S-IPATIMUP, Porto, Portugal) for MKN45 cells. We also thank Laurence Bernard-Touami and the Animal Housing ARCHE (UMS Biosit, https://biosit.univ-rennes1.fr, University of Rennes, France), and David Hardy and Magalie Tichit (Unit of Experimental Neuropathology, Institut Pasteur, Paris, France) for her technical help on the histology part and the UtechS Photonic BioImaging (Imagopole), C2RT, Institut Pasteur, supported by the French National Research Agency (France BioImaging, ANR-10–INSB–04, Investments for the Future), both as a part of the FranceBioImaging infrastructure., ANR-10-INBS-0004,France-BioImaging,Développment d'une infrastructure française distribuée coordonnée(2010), Institut Pasteur [Paris]-Université Paris Diderot - Paris 7 (UPD7)-Centre National de la Recherche Scientifique (CNRS), Centre National de la Recherche Scientifique (CNRS)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique )-Centre National de la Recherche Scientifique (CNRS)-Université de Rennes 1 (UR1), Université de Rennes (UNIV-RENNES)-Université de Rennes (UNIV-RENNES), Institut Pasteur [Paris], Institut Pasteur [Paris]-Université Paris Descartes - Paris 5 (UPD5), Università degli Studi di Firenze = University of Florence [Firenze] (UNIFI), Touati, Eliette, and Développment d'une infrastructure française distribuée coordonnée - - France-BioImaging2010 - ANR-10-INBS-0004 - INBS - VALID

Subjects
[SDV] Life Sciences [q-bio], [SDV.CAN] Life Sciences [q-bio]/Cancer, oncogenes, gastric cancer, [SDV]Life Sciences [q-bio], DNA damage, genetic instability, [SDV.CAN]Life Sciences [q-bio]/Cancer, helicobacter pylori infection, [SDV.MP.BAC] Life Sciences [q-bio]/Microbiology and Parasitology/Bacteriology, [SDV.MP.BAC]Life Sciences [q-bio]/Microbiology and Parasitology/Bacteriology
Abstract

International audience; Objective - Design - Human gastric epithelial cell lines were infected with 7.13, exposed or not to a DNA-damaging agent camptothecin (CPT), to mimic a genetic instability context. We quantified the expression of , and their target genes, we determined their subcellular localisation by immunofluorescence and examined USF1/p53 interaction. and INS-GAS mice were used to strengthen the findings in vivo and patient data examined for clinical relevance. Results - In vivo we revealed the dominant role of USF1 in protecting gastric cells against -induced carcinogenesis and its impact on p53 levels. In vitro, delocalises USF1 into foci close to cell membranes. prevents USF1/p53 nuclear built up and relocates these complexes in the cytoplasm, thereby impairing their transcriptional function. also inhibits CPT-induced USF1/p53 nuclear complexes, exacerbating CPT-dependent DNA damaging effects. Conclusion - Our data reveal that the depletion of USF1 and its de-localisation in the vicinity of cell membranes are essential events associated to the genotoxic activity of infection, thus promoting gastric carcinogenesis. These findings are also of clinical relevance, supporting USF1 expression as a potential marker of GC susceptibility.

Published
2020
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27. RNase R is associated in a functional complex with the RhpA DEAD-box RNA helicase inHelicobacter pylori

Author

Tejada-Arranz, Alejandro, primary, Matos, Rute G, additional, Quentin, Yves, additional, Bouilloux-Lafont, Maxime, additional, Galtier, Eloïse, additional, Briolat, Valérie, additional, Kornobis, Etienne, additional, Douché, Thibaut, additional, Matondo, Mariette, additional, Arraiano, Cecilia M, additional, Raynal, Bertrand, additional, and De Reuse, Hilde, additional

Published
2021
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30. The protein-protein interaction map of Helicobacter pylori

Author

Rain, Jean-Christophe, Selig, Luc, De Reuse, Hilde, Battaglia, Veronique, Reverdy, Celine, Simon, Stephane, Lenzen, Gerlinde, Petel, Fabien, Wojcik, Jerome, Schachter, Vincent, Chemama, Y., Labigne, Agnes, and Legrain, Pierre

Subjects
Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

Author(s): Jean-Christophe Rain [1]; Luc Selig [1]; Hilde De Reuse [2]; Véronique Battaglia [1]; Céline Reverdy [1]; Stéphane Simon [1]; Gerlinde Lenzen [1]; Fabien Petel [1]; Jérôme Wojcik [1]; Vincent [...]

Published
2001
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37. Design, Synthesis, and Efficacy Testing of Nitroethylene- and 7-Nitrobenzoxadiazol-Based Flavodoxin Inhibitors against Helicobacter pylori Drug-Resistant Clinical Strains and in Helicobacter pylori -Infected Mice

Author

Salillas, Sandra, Alías, Miriam, Michel, Valérie, Mahía, Alejandro, Lucía, Ainhoa, Rodrigues, Liliana, Bueno, Jessica, Galano-Frutos, Juan José, de Reuse, Hilde, Velázquez-Campoy, Adrián, Carrodeguas, José Alberto, Sostres, Carlos, Castillo, Javier, Aínsa, José Antonio, Díaz-De-Villegas, María Dolores, Lanas, Angel, Touati, Eliette, Sancho, Javier, Instituto de Biocomputación y Física de Sistemas Complejos = Institute for Biocomputation and Physics of Complex Systems (BIFI), University of Zaragoza - Universidad de Zaragoza [Zaragoza], Aragón Health Research Institute [Zaragoza, Spain], Departamento de Bioquímica y Biología Molecular y Celular [Zaragoza], Pathogenèse de Helicobacter - Helicobacter Pathogenesis, Institut Pasteur [Paris]-Université Paris Diderot - Paris 7 (UPD7)-Centre National de la Recherche Scientifique (CNRS), Centro de Investigación Biomédica en Red Enfermedades Respiratorias (CIBERES), Departamento de Microbiología, Medicina Preventiva y Salud Publica [Zaragoza], Facultad de Medicina [Zaragoza], University of Zaragoza - Universidad de Zaragoza [Zaragoza]-University of Zaragoza - Universidad de Zaragoza [Zaragoza], Fundación Agencia Aragonesa para la Investigación y el Desarrollo - ARAID [Zaragoza, Spain], Centro de Investigación Biomédica en Red en el Área temática de Enfermedades Hepáticas y Digestivas (CIBERehd), Liver Unit, Clínica Universitaria, CIBER-EHD, Instituto de Síntesis Química y Catálisis Homogénea, Departamento de Medicina, Psiquiatría y Dermatologíae [Zaragoza, Spain], J.S. was supported by grant BFU2016-78232-P (MINECO, Spain) and E45_17R (Gobierno de Aragón, Spain). A.L. was supported by grant PI11/02578 (MICINN, Spain). S.S. and A.M. are recipients of predoctoral fellowships from the Aragonese and Spanish Governments, respectively., The authors thank Dr Francis Mégraud (Bordeaux, France) for advice on culturing human Hp isolates and infecting animals with human strains., Institut Pasteur [Paris] (IP)-Université Paris Diderot - Paris 7 (UPD7)-Centre National de la Recherche Scientifique (CNRS), and Fundación Agencia Aragonesa para la Investigación y el Desarrollo (ARAID)

Subjects
MESH: Microbial Sensitivity Tests, MESH: Anti-Bacterial Agents / therapeutic use, MESH: Humans, MESH: Helicobacter Infections / drug therapy, [CHIM.THER]Chemical Sciences/Medicinal Chemistry, MESH: Drug Design, MESH: Anti-Bacterial Agents / toxicity, MESH: Anti-Bacterial Agents / chemical synthesis, MESH: Mice, Inbred C57BL, [SDV.MHEP.MI]Life Sciences [q-bio]/Human health and pathology/Infectious diseases, MESH: HeLa Cells, MESH: Animals, MESH: Oxadiazoles / chemical synthesis, MESH: Helicobacter pylori / drug effects, MESH: Oxadiazoles / toxicity, MESH: Flavodoxin / antagonists & inhibitors, MESH: Female, MESH: Oxadiazoles / therapeutic use
Abstract

International audience; Helicobacter pylori (Hp) infection is the main cause of peptic ulcer and gastric cancer. Hp eradication rates have fallen due to increasing bacterial resistance to currently used broad-spectrum antimicrobials. We have designed, synthesized, and tested redox variants of nitroethylene- and 7-nitrobenzoxadiazole-based inhibitors of the essential Hp protein flavodoxin. Derivatives of the 7-nitrobenzoxadiazole lead, carrying reduced forms of the nitro group and/or oxidized forms of a sulfur atom, display high therapeutic indexes against several reference Hp strains. These inhibitors are effective against metronidazole-, clarithromycin-, and rifampicin-resistant Hp clinical isolates. Their toxicity for mice after oral administration is low, and, when administered individually at single daily doses for 8 days in a mice model of Hp infection, they decrease significantly Hp gastric colonization rates and are able to eradicate the infection in up to 60% of the mice. These flavodoxin inhibitors constitute a novel family of Hp-specific antimicrobials that may help fight the constant increase of Hp antimicrobial-resistant strains.

Published
2019
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48. USF1 defect drives p53 degradation during Helicobacter pylori infection and accelerates gastric carcinogenesis

Author

Costa, Lionel, primary, Corre, Sébastien, additional, Michel, Valérie, additional, Le Luel, Krysten, additional, Fernandes, Julien, additional, Ziveri, Jason, additional, Jouvion, Gregory, additional, Danckaert, Anne, additional, Mouchet, Nicolas, additional, Da Silva Barreira, David, additional, Torres, Javier, additional, Camorlinga, Margarita, additional, D'Elios, Mario Milco, additional, Fiette, Laurence, additional, De Reuse, Hilde, additional, Galibert, Marie-Dominique, additional, and Touati, Eliette, additional

Published
2019
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50. From array-based hybridization of Helicobacter pylori isolates to the complete genome sequence of an isolate associated with MALT lymphoma

Author

Mégraud Francis, Lamarque Dominique, Boneca Ivo, De Reuse Hilde, Courillon-Mallet Anne, Ruskoné-Foumestraux Anne, Burucoa Christophe, Ma Laurence, Lajus Aurélie, Rouy Zoé, Coppée Jean-Yves, Dillies Marie-Agnès, Creno Sophie, Lehours Philippe, Thiberge Jean-Michel, Boursaux-Eude Caroline, Delchier Jean-Charles, Médigue Claudine, Bouchier Christiane, Labigne Agnès, and Raymond Josette

Subjects
Biotechnology, TP248.13-248.65, Genetics, QH426-470
Abstract

Abstract Background elicobacter pylori infection is associated with several gastro-duodenal inflammatory diseases of various levels of severity. To determine whether certain combinations of genetic markers can be used to predict the clinical source of the infection, we analyzed well documented and geographically homogenous clinical isolates using a comparative genomics approach. Results A set of 254 H. pylori genes was used to perform array-based comparative genomic hybridization among 120 French H. pylori strains associated with chronic gastritis (n = 33), duodenal ulcers (n = 27), intestinal metaplasia (n = 17) or gastric extra-nodal marginal zone B-cell MALT lymphoma (n = 43). Hierarchical cluster analyses of the DNA hybridization values allowed us to identify a homogeneous subpopulation of strains that clustered exclusively with cagPAI minus MALT lymphoma isolates. The genome sequence of B38, a representative of this MALT lymphoma strain-cluster, was completed, fully annotated, and compared with the six previously released H. pylori genomes (i.e. J99, 26695, HPAG1, P12, G27 and Shi470). B38 has the smallest H. pylori genome described thus far (1,576,758 base pairs containing 1,528 CDSs); it contains the vacAs2m2 allele and lacks the genes encoding the major virulence factors (absence of cagPAI, babB, babC, sabB, and homB). Comparative genomics led to the identification of very few sequences that are unique to the B38 strain (9 intact CDSs and 7 pseudogenes). Pair-wise genomic synteny comparisons between B38 and the 6 H. pylori sequenced genomes revealed an almost complete co-linearity, never seen before between the genomes of strain Shi470 (a Peruvian isolate) and B38. Conclusion These isolates are deprived of the main H. pylori virulence factors characterized previously, but are nonetheless associated with gastric neoplasia.

Published
2010
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