Dissertations / Theses: 'Infections à Helicobacter'

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Houben, Martinus Henricus Maria Gerardus. "Clinical aspects in Helicobacter pylori infections." [S.l. : Amsterdam : s.n.] ; Universiteit van Amsterdam [Host], 2000. http://dare.uva.nl/document/81155.

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Kivi, Mårten. "Aspects of Helicobacter pylori transmission /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-422-8/.

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Rader, Bethany Anne. "Autoinducer-2 regulation of motility in Helicobacter pylori /." view abstract or download file of text, 2006. http://proquest.umi.com/pqdweb?did=1251819321&sid=6&Fmt=2&clientId=11238&RQT=309&VName=PQD.

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Thesis (Ph. D.)--University of Oregon, 2006.
Typescript. Includes vita and abstract. Includes bibliographical references (leaves 80 - 90). Also available for download via the World Wide Web; free to University of Oregon users.

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4

Garrett, June Kazumi. "Inhibition of Helicobacter pylori by Wild Blueberry Phenolics." Fogler Library, University of Maine, 2009. http://www.library.umaine.edu/theses/pdf/GarrettJK2009.pdf.

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5

Wong, Wai-man Raymond, and 王衛民. "The pathology, diagnosis and treatment of helicobacter pylori infection." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2001. http://hub.hku.hk/bib/B23331707.

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6

Enroth, Helena. "Helicobacter pylori : bacterial diversity and human disease : microbiological and epidemiological studies with special reference to gastric cancer /." Stockholm, 1999. http://diss.kib.ki.se/1999/91-628-3673-0/.

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Myles, Matthew Howard. "Helicobacter hepaticus induced gene dysregulation in mice /." Free to MU Campus, others may purchase, 2004. http://wwwlib.umi.com/cr/mo/fullcit?p3137733.

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8

Wanken, Amy Elizabeth. "Helicobacter pylori colonization of the mouse gastric mucosa the Entner-Doudoroff pathway and development of a promoter-trapping system /." Columbus, Ohio : Ohio State University, 2004. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1059079727.

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Thesis (Ph. D.)--Ohio State University, 2003.
Title from first page of PDF file. Document formatted into pages; contains xiii, 145 p.; also includes graphics (some col.). Includes abstract and vita. Advisor: Kathryn Eaton, Dept. of Veterinary Biosciences. Includes bibliographical references (p. 130-145).

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Ben, Cheikh M'Hamed Laurence De Korwin Jean-Dominique. "Diagnostic en médecine générale." [S.l] : [s.n], 2003. http://www.scd.uhp-nancy.fr/docnum/SCDMED_T_2003_GONDA_BEN_CHEIKH_M_HAMED_LAURENCE.pdf.

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Nguyen, Thi Viet Ha. "Diagnosis and treatment of Helicobacter pylori infection in Vietnamese children." Stockholm : Karolinska institutet, 2009. http://diss.kib.ki.se/2009/978-91-7409-717-7/.

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11

Outlioua, Ahmed. "Exploration des cytokines pro-inflammatoires et de l’inflammasome NLRP3 dans les infections intracellulaires : cas de H. pylori et des virus à ARN Gastric IL-1β, IL-8, and IL-17A expression in Moroccan patients infected with Helicobacter pylori may be a predictive signature of severe pathological stages RNA viruses promote activation of the NLRP3 inflammasome through cytopathogenic effect-induced potassium efflux The heme-regulated inhibitor is a cytosolic sensor of protein misfolding that controls innate immune signaling The Role of Optineurin in Antiviral Type I Interferon Production Possible introduction of Leishmania tropica to urban areas determined by epidemiological and clinical profiles of patients with cutaneous leishmaniasis in Casablanca (Morocco)." Thesis, université Paris-Saclay, 2021. http://www.theses.fr/2021UPASL029.

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Helicobacter pylori (H. pylori) est une bactérie qui infecte l’estomac et induit une gastrite inflammatoire, qui peut être chronique et évoluer vers un cancer gastrique. La sévérité de l’infection et son évolution clinique sont associées aux différents facteurs notamment le statut immunitaire de l’hôte. La réponse inflammatoire initiale à l'infection à H. pylori entraîne la sécrétion d'un large panel de cytokines, notamment l'interleukine-1β (IL-1β), l'IL-8 et l'IL-17A. qui semblent jouer un rôle clé dans l'initiation et la progression du cancer gastrique. Parmi ces cytokines, l'IL-1β est une cytokine clé au cours de l’infection à H. pylori dont l’expression est étroitement associée à l'inflammation gastrique et à la carcinogenèse. La production de cette cytokine dépend de l'activation de l'inflammasome, en particulier l'inflammasome NLRP3. Ce dernier, responsable de l’activation des processus inflammatoires, est essentiel pour le maintien de l'homéostasie contre diverses infections pathogènes telles les infections bactérienne et virale.L’objectif général de ce travail est i) d’étudier l’expression et le polymorphisme des gènes de cytokines comme IL-1β, IL-17 et IL-8 chez des patients marocains infectés par H. pylori. ii) explorer l’activation de l'inflammasome NLRP3 par H. pylori et déterminer les mécanismes impliqués dans l'activation de ce complexe par des virus à ARN ; connus comme des activateurs définis de NLRP3.Nos résultats ont souligné une prévalence élevée de H. pylori et ont mis en évidence une signature cytokinique : elle peut prédire la métaplasie au cours de la progression de l'infection à H. pylori impliquant une diminution de l’expression de l'IL17A dans l’antre et une augmentation de l’expression de l'IL-1β dans le fundus. Plus particulièrement, les polymorphismes génétiques de l’IL-1β (IL-1β -31 et -511) ne semblent pas influencer l’expression de l’IL-1β de manière significative.Au regard des difficultés rencontrés pour l’isolement et la culture de H. pylori, nous avons utilisé le LPS de H. pylori pour stimuler l’inflammasome. Nos résultats montrent que la transfection des cellules in vitro par le LPS bactérien induit la production de l’IL-1β qui semble être modulée par la caspase 4, NOD1 et NOD2. Par ailleurs, bien qu’il soit clairement établi que les virus à ARN induisent l’activation de l’inflammasome NLRP3, les mécanismes par lesquels ces virus induisent la production d'IL-1β ne sont pas bien compris et restent à confirmer. Les résultats de cette partie du travail ont montré que la réplication des virus à ARN cytopathogènes tels que le virus de la stomatite vésiculaire (VSV) ou le virus de l'encéphalomyocardite (EMCV) induit une mort cellulaire lytique conduisant à un efflux de potassium qui déclenche l'activation de l'inflammasome NLRP3. Ainsi, les virus à forte capacité de réplication et qui ont un effet cytopathique sont capables d'induire l'activation de la caspase-1 conduisant à la production d'IL-1β. A l'inverse, les virus qui induisent une très bonne réponse IFN de type I sont de très mauvais inducteurs de l'inflammasome NLRP3.Une meilleure compréhension de l’activation de l’inflammasome pourrait aider dans la mise au point de stratégies thérapeutiques ciblées utilisables dans la lutte contre les infections bactérienne et virale.Mots clés : Helicobacter pylori, inflammation, inflammasome NLRP3, IL-1β, virus à ARN
Helicobacter pylori (H. pylori) is a bacteria that infects the stomach and induces inflammatory gastritis, which can be chronic and progress to gastric cancer. The severity of the infection and its clinical course are associated with various factors including the immune status of the host. The initial inflammatory response to H. pylori infection results in the secretion of a wide range of cytokines, including interleukin-1β (IL-1β), IL-8 and IL-17A. which appear to play a key role in the initiation and progression of gastric cancer. Among these cytokines, IL-1β is a key cytokine during H. pylori infection whose expression is associated with gastric inflammation and carcinogenesis. The production of this cytokine depends on the activation of the inflammasome, in particular the NLRP3 inflammasome. The latter, responsible of the activation of inflammatory processes, is essential for the maintenance of homeostasis against various pathogenic infections such as bacterial and viral infections.The general objective of this work is i) to study the expression and polymorphism of genes for cytokines such as IL-1β, IL-17 and IL-8 in Moroccan patients infected with H. pylori. ii) explore the activation of the NLRP3 inflammasome by H. pylori and determine the mechanisms involved in the activation of this complex by RNA viruses; known as defined activators of NLRP3.Our results underlined a high prevalence of H. pylori and demonstrated a cytokine signature: it can predict metaplasia during the progression of H. pylori infection involving a decrease in IL17A expression in the antrum and increased expression of IL-1β in the fundus. In particular, the genetic polymorphisms of IL-1β (IL-1β -31 and -511) do not appear to influence IL-1β expression significantly.In view of the difficulties encountered in isolating and culturing H. pylori, we used LPS from H. pylori to stimulate the inflammasome. Our results show that the transfection of cells in vitro with bacterial LPS induces the production of IL-1β which appears to be modulated by caspase 4, NOD1 and NOD2. Furthermore, while it is clearly established that RNA viruses induce activation of the NLRP3 inflammasome, the mechanisms by which these viruses induce IL-1β production are not well understood and remain to be confirmed. The results of this part of the work showed that the replication of cytopathogenic RNA viruses such as vesicular stomatitis virus (VSV) or encephalomyocarditis virus (EMCV) induces lytic cell death leading to an efflux of potassium which triggers activation of the NLRP3 inflammasome. Thus, viruses with a high replication capacity and which have a cytopathic effect are capable of inducing the activation of caspase-1 leading to the production of IL-1β. Conversely, viruses which induce type I IFN response are very poor inducers of the NLRP3 inflammasome.A better understanding of the activation of the inflammasome could help in the development of targeted therapeutic strategies for use in the fight against bacterial and viral infections.Key words: Helicobacter pylori, inflammation, NLRP3 inflammasome, IL-1β, RNA virus

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12

Chu, Kent-man. "Helicobacter pylori infection and gastroduodenal ulcer disease." Hong Kong : University of Hong Kong, 2001. http://sunzi.lib.hku.hk/hkuto/record.jsp?B23636555.

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13

Olfat, Farzad O. "Helicobacter pylori - bacterial adhesion and host response /." Umeå : Univ, 2003. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-133.

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Wong, Chun-yu Benjamin. "Helicobacter pylori : related diseases in the Chinese /." Hong Kong : University of Hong Kong, 2000. http://sunzi.lib.hku.hk/hkuto/record.jsp?B22226977.

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15

朱建民 and Kent-man Chu. "Helicobacter pylori infection and gastroduodenal ulcer disease." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2001. http://hub.hku.hk/bib/B23685426.

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16

Wallace, Robyn A. "The biopsychosocial implications of helicobacter pylori infection in adults with intellectual disability /." St. Lucia, Qld, 2002. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe16438.pdf.

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17

Wheeldon, Thục-Uyên. "Management of Helicobacter pylori infection in Vietnam /." Stockholm, 2004. http://diss.kib.ki.se/2004/91-7349-876-9/.

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18

Sun, Yi-Qian. "Experimental Helicobacter pylori infection in an animal model : gastric microflora, morpho-functional development, mucosal barrier function, and effects of antioxidants in Mongolian gerbils /." Linköping : Univ, 2004. http://www.bibl.liu.se/liupubl/disp/disp2004/med876s.pdf.

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19

Fall, Katja. "Medical interventions and gastric cancer risk : an observational approach /." Stockholm, 2004. http://diss.kib.ki.se/2004/91-7349-905-6/.

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20

Unge, Peter. "Pharmacological therapy of Helicobacter pylori infection /." Linköping : Univ, 2002. http://www.bibl.liu.se/liupubl/disp/disp2002/med734s.pdf.

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21

Paillé, Pascal. "Hélicobacter Pylori et gastrite chronique chez l'adulte jeune, essai d'utilisation du "Sydney system"." Bordeaux 2, 1991. http://www.theses.fr/1991BOR2M187.

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22

Thomas, Theodore Seth. "Development of a capillary based helicobacter hepaticus biosensor." Diss., Columbia, Mo. : University of Missouri-Columbia, 2006. http://hdl.handle.net/10355/4572.

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Thesis (M.S.) University of Missouri-Columbia, 2006.
The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. Title from title screen of research.pdf file viewed on (June 27, 2007) Includes bibliographical references.

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23

Daugule, Ilva. "Helicobacter pylori infection among children in Riga, Latvia /." Stockholm, 2007. http://diss.kib.ki.se/2007/978-91-7140-630-9/.

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24

Petersson, Fredrik. "Chronic gastritis in a sample of the general population : Helicobacter pylori infection, metaplastic transformation, epithelial proliferation, p53- and p21 expression and antral mucosal gastrin content with reference to gastric carcinoma development /." Linköping : Univ, 2004. http://www.bibl.liu.se/liupubl/disp/disp2004/med855s.pdf.

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25

Renou-Piton, Béatrice. "Prévalence de l'infection à Helicobacter pylori dans une population de 249 patients souffrant de dyspepsie fonctionnelle." Bordeaux 2, 1999. http://www.theses.fr/1999BOR23107.

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26

Petersson, Christoffer. "Characterisation of surface traits of Helicobacter pylori and their role in the infectious process /." Linköping : Univ, 2003. http://www.bibl.liu.se/liupubl/disp/disp2003/med805s.pdf.

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27

Nayak, Arun Kumar. "Stability and quantitative surveillance of Helicobacter pylori and Campylobacter jejuni in environmental waters by real time qPCR." Diss., Connect to online resource - MSU authorized users, 2008.

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Wen, Sicheng. "The mucosal immune response against Helicobacter pylori infection /." Stockholm, 2007. http://diss.kib.ki.se/2007/978-91-7357-033-6/.

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Warren, John Robin. "The discovery and pathology of H pylori /." Title page and contents only, 1999. http://web4.library.adelaide.edu.au/theses/09MD/09mdw289.pdf.

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30

Milgrom, Sarah Allison. "Seroprevalence of Helicobacter pylori in Rural Ecuador." Yale University, 2009. http://ymtdl.med.yale.edu/theses/available/etd-03292009-172126/.

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Helicobacter pylori infection causes chronic type B gastritis, peptic ulcer disease, gastric adenocarcinoma, and gastric mucosa-associated lymphoid tumor. Infection with H. pylori is common in parts of the developing world. The Clínica Misional Nuestra Señora de Guadalupe serves indigenous people of the Ecuadorian Amazon. At the clinic, gastritis is a common diagnosis that is based solely on reported symptoms and is presumed to be due to H. pylori infection. Additionally, gastric cancer, a corollary of H. pylori infection, is the leading cause of cancer deaths in Ecuador and, thus, an important public health concern. To the best of our knowledge, the prevalence of H. pylori infection among the inhabitants of rural Ecuador has never been assessed. The primary aim of this study was to determine the seroprevalence of H. pylori in this population. We compared rates of seropositivity among patients with and without symptoms suggestive of gastritis and among patients who reported untreated and exclusively treated water consumption. Additionally, a sampling of children was tested to begin to assess the age of serological conversion. Using the Quidel QuickVue H. pylori gII test, we found near universal seropositivity among adults aged 18 to 65 years (117/120 = 98%) and among children aged 2 to 18 years (13/14 = 93%). Given the high prevalence of H. pylori and its complications in rural Ecuador, this population may benefit from intervention to eradicate the bacterium. However, there is a lack of evidence to inform management decisions. There is a need for studies with large numbers of patients and long-term follow-up to assess the costs and benefits of population-based treatment.

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Boublil, Laurence Yae͏̈l. "Maladie ulcéreuse : physiopathologie, traitements ; rôle d'hélicobacter pylori." Paris 5, 1998. http://www.theses.fr/1998PA05P006.

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Bartfeld, Sina. "NF-kappaB activation in infections with Helicobacter pylori or Legionella pneumophila." Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2009. http://dx.doi.org/10.18452/15939.

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Bakterielle Infektionen aktivieren den Transkriptionsfaktor NF-κB. Dies trägt sowohl zur Immunantwort, als auch zum Überleben der Wirtszellen bei. In Infektionen mit dem Bakterium Helicobacter pylori stellt diese doppelte Funktion einen mechanistischen Link zwischen der chronischen Entzündung und der Krebsentstehung dar. Für das intrazelluläre Bakterium Legionella pneumophila ist das Überleben der Wirtszelle notwendig für die Vermehrung. Bisher sind jedoch bei beiden Infektionen die Signalwege, die zur NF-κB-Aktivierung führen, nicht ausreichend untersucht. Um NF-κB analysieren zu können, wurden hier monoklonale Zelllinien hergestellt, die ein Fusionsprotein der NF-κB-Untereinheit p65 mit GFP stabil exprimieren. Die Kerntranslokation von p65-GFP kann mit Fluoreszenz-Mikroskopie visualisiert und mit automatischer Bildanalyse quantifiziert werden. Mit dieser Methode konnte zum ersten Mal eine durch ein Bakterium induzierte Oszillation von p65-GFP gezeigt werden. In einem RNAi-basierten Hochdurchsatzscreen wurde diese Methode eingesetzt um neue Faktoren im NF-κB-Signalweg zu identifizieren. Dabei wurde die Infektion mit H. pylori mit den Induktoren TNFα und IL-1β verglichen. Insgesamt wurden 24 Regulatoren identifiziert. Die Identifikation dieser Faktoren vertieft nicht nur unser Verständnis des NF-κB-Signalweges, sondern bietet auch neue molekulare Ziele für mögliche zukünftige Therapien. Bei der detaillierten Analyse der L. pneumophila-induzierten NF-κB-Aktivierung konnte ein einzigartiger, zwei-phasiger Ablauf gezeigt werden. Zunächst verursachte bakterielles Flagellin eine starke, aber kurze Aktivierung. Später war p65 dauerhaft über Stunden im Kern lokalisiert, was eng an die Replikation der Bakterien gekoppelt war. Da die kontinuierliche Kernlokalisation für Transkriptionsfaktoren der NF-κB Familie sehr ungewöhnlich ist, könnte dies ein Hinweis für eine Manipulation durch das Bakterium sein, um das Überleben der Wirtszelle zu sichern.
Infection with pathogens leads to activation of the transcription factor NF-κB. This contributes both to the immune response as well as survival of host cells. In infection with the bacterium Helicobacter pylori, this dual function provides a mechanistic link between the chronic inflammation and cancer development. In infection with the intracellular pathogen Legionella pneumophila, the survival oft he host cell is necessary for replication. However, in both infections, the signaling pathways leading to NF-κB activation are not well understood. Here, in order to investigate NF-κB activation, monoclonal cell lines were generated that stably express the NF-κB subunit p65 fused to GFP. Nuclear translocation of p65-GFP can be visualized by fluorescence microscopy and quantified by software-based picture analysis. Using this technology, oscillations of p65-GFP nuclear translocation could be shown after H. pylori infection. To identify new factors important for NF-κB activation, the new assay was used to conduct an RNAi-based screen. In the screen, infection with H. pylori was compared to induction with the cytokines TNFα and IL-1β. In total, 24 key regulators for NF-κB were identified. The identification of these factors broadens our understanding of NF-κB signaling and could provide targets for future therapies. Finally, detailed observation of NF-κB activation induced by L. pneumophila in single cells revealed a unique, biphasic NF-κB activation. During the first hours, bacterial flagellin induced strong but transient activation. Then, p65 translocated continuously to the nucleus over hours without oscillation. Testing an array of bacterial mutants, a tight link between bacterial replication and continuous NF-κB activation could be shown. Because this continuous nuclear localization is very unusual for a transcription factor of the NF-κB family, this indicates that L. pneumophila could manipulate NF-κB to ensure host cell survival.

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Hoang, Thi Thu Ha. "Serodiagnosis and seroprevalence of Helicobacter pylori infection in Vietnam /." Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-918-1/.

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Nilsson, Christina. "Genome-plasticity and adaptation in Helicobacter pylori /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-189-X/.

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Khoder, Ghalia. "Biomarqueurs protéomiques du pathogène gastrique Helicobacter pylori." Poitiers, 2008. http://www.theses.fr/2008POIT1803.

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Bäckhed, Fredrik. "Role of toll-like receptors in host responses to mucosal bacterial infections /." Stockholm, 2002. http://diss.kib.ki.se/2002/91-7349-367-8/.

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Rigot, Agnès. "Hélicobacter pylori et gastrites chez l'enfant : à propos de 14 observations." Bordeaux 2, 1991. http://www.theses.fr/1991BOR23113.

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Bourzac, Kevin. "A molecular and cellular investigation of Helicobacter pylori's cag pathogenicity island and interactions with host cells /." view abstract or download file of text, 2006. http://proquest.umi.com/pqdweb?index=0&did=1251819291&SrchMode=1&sid=1&Fmt=2&VInst=PROD&VType=PQD&RQT=309&VName=PQD&TS=1181341914&clientId=11238.

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Thesis (Ph. D.)--University of Oregon, 2006.
Typescript. Includes vita and abstract. Includes bibliographical references (leaves 80-91). Also available for download via the World Wide Web; free to University of Oregon users.

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Talbi, Patrice. "Macrolides et éradication de Hélicobacter pylori." Bordeaux 2, 1994. http://www.theses.fr/1994BOR23066.

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Jansson, Rehnberg Ann-Sofie. "Diagnostic methods in helicobacter pylori infection : development, evaluation and application /." Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-993-9/.

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Belair, Cédric. "Rôle des microARNs dans les infections bactériennes chez l’Homme : le modèle Helicobacter pylori." Thesis, Bordeaux 2, 2010. http://www.theses.fr/2010BOR21768/document.

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Les microARNs, régulateurs post-transcriptionnels de l’expression des gènes eucaryotes, sont impliqués dans la défense contre les pathogènes. Afin de favoriser leur multiplication, les virus et les bactéries ont développé des stratégies pour altérer la voie des miRNAs. Dans ce travail, nous avons montré que Helicobacter pylori, une bactérie responsable chez l’Homme de pathologies gastriques sévères, telles que l’ulcère ou le cancer, réprime un cluster de microARNs spécifique des cellules souches embryonnaires dans une lignée épithéliale gastrique. En utilisant une technique de séquençage à haut débit, nous avons identifié miR-372 comme le miRNA le plus exprimé dans cette lignée gastrique. Avec miR-373, miR-372 permet la prolifération cellulaire réprimant l’expression d’un inhibiteur du cycle cellulaire, the LArge Tumor Suppressor 2 (LATS2). Au cours de l’infection par H. pylori, l’expression de miR-372&373 est réprimée, provoquant une accumulation de LATS2 et un arrêt du cycle cellulaire. De manière importante, la répression de ces miRNAs est dépendante de la translocation de l’effecteur bactérien CagA dans la cellule hôte. Ces données constituent un nouvel exemple d’interaction hôte-pathogène impliquant les miRNAs et ont identifié le couple LATS2/miR-372&373 comme un mécanisme inattendu dans l’arrêt du cycle cellulaire observé au cours de l’infection. Ce mécanisme pourrait refléter l’inhibition de l’auto-renouvellement de l’épithélium gastrique, processus impliqué dans la défense contre les infections bactériennes
MicroRNAs, post-transcriptionnal regulators of eukaryotic gene expression, are implicated in host defense against pathogens. Viruses and bacteria have evolved strategies to suppress miRNA functions with the aim to establish a sustainable infection. In this work, we report that Helicobacter pylori, a bacterium responsible for severe human gastric inflammatory diseases and cancers, down-regulates an embryonic-specific microRNAs cluster in a gastric epithelial cell line. We reveal by using a deep sequencing approach that hsa-miR-372 is the most abundant miRNA expressed in this gastric cell line where, together with hsa-miR-373, it promotes cell proliferation by silencing the expression of a cell cycle inhibitor, the LArge Tumor Suppressor 2 (LATS2). Upon H. pylori infection, miR-372&373 synthesis is inhibited, leading to the derepression of LATS2 and thus, to a cell cycle arrest at the G1/S transition. Importantly, this down-regulation of a specific cell cycle-regulating microRNA is dependent on the translocation of the bacterial effector CagA into the host cells. These data constitute a novel example of host-pathogen interplay involving microRNAs and unveil the couple LATS2/miR-372&373 as an unexpected mechanism in infection-induced cell cycle arrest in proliferating gastric cells which may be relevant of inhibition of gastric epithelium renewal, a major host defense mechanism against bacterial infections

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42

Wong, Chun-yu Benjamin, and 王振宇. "Helicobacter pylori: related diseases in the Chinese." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2000. http://hub.hku.hk/bib/B31981732.

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43

Masso, Zelie Flavienne. "Assessing cardiotonic steroids involvement in hypertensive rat models with Helicobacter pylori infections." Diss., University of Pretoria, 2020. http://hdl.handle.net/2263/75537.

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Introduction: Hypertension is an important public health challenge worldwide, being the leading cause of cardiovascular disease, morbidity and mortality. It is particularly prevalent in people in sub-Saharan Africa, especially in urban areas. There is an urgent need to develop strategies to prevent, detect, treat, and control hypertension effectively in the African region. Helicobacter pylori, a gram-negative bacterium responsible for many gastric disorders worldwide, has been associated with hypertension in some previous studies; where blood pressure of patients with Helicobacter pylori infection did not subside after hypertensive treatment, when compared to patients without Helicobacter pylori infections. This effect was suggested to be due to Helicobacter pylori produced and modified cardiotonic steroids that are found in elevated concentrations in hypertensive patients. Cardiotonic steroids are positive inotropic agents which are known to increase blood pressure. A sensitive analytical method is needed to detect and quantify the low concentrations of cardiotonic steroids in biological samples. Materials and Methods: An extraction method was optimised using reversed phase Solid Phase Extraction. A targeted liquid chromatography tandem mass spectrometry method using an Agilent binary series 1100/1200 LC system with a Kinetex C18 RP column (100 x 2.1 mm, 2.6 µm) coupled to a Sciex 4000QTRAP tandem mass spectrometer was developed and validated for the detection and quantitation of 9 different cardiotonic steroids in both solvent and whole blood. The method was validated according to the International Conference on Harmonization guidelines with regards to precision, accuracy, sensitivity, selectivity, linearity, range, limit of detection, limit of quantification, reproducibility, recovery, carry-over and stability. Media from Helicobacter pylori cultures and faecal samples from human and different normo- and hypertensive rat strains were analysed. Data analysis was performed with Analyst® Software (version 1.5.2) and multiple t-test and Kruskal Wallis test using GraphPad Prism 8 software. Results and Discussion: The calibration curves of tested cardiotonic steroids were linear over a concentration range of 0.1-40 ng/mL with coefficients of determination greater than 0.990 except for telocinobufagin. The analytical method was selective with an estimated limit of detection and limit of quantification between 0.02-0.5 ng/mL and 0.1-2 ng/mL respectively. All tested cardiotonic steroids showed good recovery of over 70%. Accuracy and precision were found to be within acceptable limits of 15% and 20% at lowest limit of quantification for almost all the analytes and their stability in blood and solvent at room temperature, 4°C, -20°C and -80°C was tested for a month. Cardiotonic steroids were detected in Helicobacter pylori cultures and faecal samples with the exception of ouabain and proscillaridin A which were not detected at all. Although Helicobacter pylori were shown to produce cardiotonic steroids in vitro, no evidence of the effect of Helicobacter pylori on cardiotonic steroids production was detected in different normo- and hypertensive rat groups. Conclusion: The quantitative analytical method was successfully validated, over expected in vivo concentration ranges for 8 different cardiotonic steroids. The extraction and analytical methods were both successfully applied to Helicobacter pylori cultures and faecal rat samples where cardiotonic steroids were detected.
Dissertation (MSc)--University of Pretoria 2020.
National Research Foundation Student bursary
Pharmacology
MSc (Pharmacology)
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44

Miendjé, Deyi Véronique Yvette. "Contribution au management de l'infection à Helicobacter pylori en Belgique." Doctoral thesis, Universite Libre de Bruxelles, 2011. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/209925.

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Peu étudiée et méconnue, initialement décrite au début du XXe siècle, Helicobacter pylori fut redécouverte en 1982 par deux chercheurs australiens, JR Warren et BJ Marshall. Ils soutinrent que la plupart des ulcères gastro-duodénaux étaient causés par cette bactérie, et non par le stress ou la nourriture épicée, comme pensé auparavant. Cette découverte révolutionna le monde de la gastroentérologie et leur valut le prix Nobel de physiologie et de médecine 2005. Environ la moitié de la population mondiale est colonisée par H. pylori au niveau de l'estomac. Dans 10 à 20% des cas, l'infection peut évoluer vers un ulcère gastro-duodénal et dans certains cas vers une transformation maligne. Cette infection se soigne classiquement à l'aide d'une trithérapie associant 2 antibiotiques à un inhibiteur de la pompe à protons pour neutraliser l'acidité gastrique.

Notre travail de recherche a consisté à analyser la proportion de patients infectés par H. pylori dans une cohorte de plus de 22.000 patients, issus de divers groupes ethniques, vivant en Belgique. Ces souches de H. pylori, isolées dans notre laboratoire, à partir des biopsies gastriques, ont aussi servi à une étude pour suivre l'évolution de la résistance aux antibiotiques ces 20 dernières années afin de proposer des améliorations de la prise en charge thérapeutique de l'infection à H. pylori en Belgique.
Doctorat en Sciences biomédicales et pharmaceutiques
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Rapp, Nathalie. "Gastrites chroniques et formes folliculaires associées à hélicobacter pylori : aspects histologiques et endoscopiques : étude prospective de 445 observations." Bordeaux 2, 1993. http://www.theses.fr/1993BOR2M139.

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Held, Maria. "Epidemiological studies of Helicobacter pylori and its relation to cancer and precancerous lesions in the upper gastrointestinal tract /." Stockholm, 2004. http://diss.kib.ki.se/2004/91-7349-944-7/.

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47

Laharie, David. "Bactéries du genre Helicobacter et inflammation intestinale : approche expérimentale et humaine." Bordeaux 2, 2006. http://www.theses.fr/2006BOR21361.

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Les bactéries du genre Helicobacter pourraient être impliquées dans la pathogénie de la maladie de Crohn. L(objet de cette thèse était d'étudier leur rôle au cours de l'inflammation intestinale chronique. Des travaux menés chez l'animal ont permis d'étudier l'effet de 2 souches probiotiques et de leur surnageant puis du rebamipide, agent mucoprotecteur renforçant la barrière épithéliale, sur un modèle de colite développée par les souris déficientes en interleukine-10 et potentialisée par l'infection par Helicobacter hepaticus. L'effet pro-inflammatoire exercé par une espèce émergente en pathologie humaine, Helicobacter pullorum, a été évalué sur des lignées cellulaires intestinales. Il semble inpliquer la voie du NF-kB et pourrait être lié à son lipopolysaccharide. Les résultats préliminaires d'une étude cas-témoin, transversale et multicentrique française suggèrent que les bactéries du genre Helicobacter pourraient être associées à la récidive post-opératoire de la maladie de Crohn
Helicobacter species could be involved in the pathogenesis of Crohn's disease. The aim of this work was to study their effect on chronic intestinal inflammation. First, two probiotic strains or their supernatant and rebamipide, an original molecule with mucosal protective properties improving the epithelial barrier, were studied on the murine model of colitis observed on interleukin-10 deficient mice infected with Helicobacter hepaticus. Second, the pro-inflammatory effect of emerging pathogen specie, Helicobacter pullorum, was assessed on epithelial cell lines. It could be lipopolysaccharide-induced, involving NF-kB pathway. Third, preliminary results of a wide prospective French case-control study suggested that Helicobacter species could be associated with Crohn's disease post-operative recurrence

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Engberg, Jørgen. "Contributions to the epidemiology of campylobacter infections : a review of clinical and microbiological studies /." København : Lægeforeningens Forlag, 2006. http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&doc_number=015052341&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA.

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Blancan, Évelyne. "Dépistage de l'infection à hélicobacter pylori chez des enfants présentant des douleurs abdominales récurrentes : étude prospective portant sur 86 cas." Bordeaux 2, 1993. http://www.theses.fr/1993BOR2M131.

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Olive, Claude. "Séroépidémiologie de l'infection à hélicobacter pylori dans l'ile de la Réunion." Bordeaux 2, 1991. http://www.theses.fr/1991BOR23028.

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