Dissertations / Theses on the topic 'Helicobacter pylori infections'
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Kivi, Mårten. "Aspects of Helicobacter pylori transmission /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-422-8/.
Full textHouben, 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.
Full textGarrett, 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.
Full textRader, 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.
Full textTypescript. 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.
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.
Full textTitle 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).
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.
Full textBen, 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.
Full textChu, 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.
Full textUnge, Peter. "Pharmacological therapy of Helicobacter pylori infection /." Linköping : Univ, 2002. http://www.bibl.liu.se/liupubl/disp/disp2002/med734s.pdf.
Full textOlfat, Farzad O. "Helicobacter pylori - bacterial adhesion and host response /." Umeå : Univ, 2003. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-133.
Full textWong, 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.
Full text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.
Full textOutlioua, 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.
Full textHelicobacter 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
Wheeldon, Thục-Uyên. "Management of Helicobacter pylori infection in Vietnam /." Stockholm, 2004. http://diss.kib.ki.se/2004/91-7349-876-9/.
Full textNguyen, 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/.
Full textBoublil, Laurence Yae͏̈l. "Maladie ulcéreuse : physiopathologie, traitements ; rôle d'hélicobacter pylori." Paris 5, 1998. http://www.theses.fr/1998PA05P006.
Full textWallace, 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.
Full textWarren, 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.
Full textDaugule, Ilva. "Helicobacter pylori infection among children in Riga, Latvia /." Stockholm, 2007. http://diss.kib.ki.se/2007/978-91-7140-630-9/.
Full textTalbi, Patrice. "Macrolides et éradication de Hélicobacter pylori." Bordeaux 2, 1994. http://www.theses.fr/1994BOR23066.
Full textMilgrom, Sarah Allison. "Seroprevalence of Helicobacter pylori in Rural Ecuador." Yale University, 2009. http://ymtdl.med.yale.edu/theses/available/etd-03292009-172126/.
Full textRigot, Agnès. "Hélicobacter pylori et gastrites chez l'enfant : à propos de 14 observations." Bordeaux 2, 1991. http://www.theses.fr/1991BOR23113.
Full textNilsson, Christina. "Genome-plasticity and adaptation in Helicobacter pylori /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-189-X/.
Full textWen, Sicheng. "The mucosal immune response against Helicobacter pylori infection /." Stockholm, 2007. http://diss.kib.ki.se/2007/978-91-7357-033-6/.
Full textKhoder, Ghalia. "Biomarqueurs protéomiques du pathogène gastrique Helicobacter pylori." Poitiers, 2008. http://www.theses.fr/2008POIT1803.
Full textWong, 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.
Full textRapp, 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.
Full textBourzac, 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.
Full textTypescript. 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.
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.
Full textPaillé, Pascal. "Hélicobacter Pylori et gastrite chronique chez l'adulte jeune, essai d'utilisation du "Sydney system"." Bordeaux 2, 1991. http://www.theses.fr/1991BOR2M187.
Full textMassiere, Jessica. "La transition épithélio-mésenchymateuse dans les cellules épithéliales gastriques : rôle des microARN régulés par Helicobacter pylori." Thesis, Bordeaux 2, 2011. http://www.theses.fr/2011BOR21835/document.
Full textMicroRNA are small noncoding RNA that post-transcriptionally regulate gene expression. Due to their high regulator potential, a change in their expression may lead to the emergence of diseases such as cancer or inhibition of defense mechanisms against pathogens. Our aim is to characterize the role of miRNA in the response of gastric eptithelial cells to Helicobacter pylori (H. pylori). Indeed, H. pylori promote gastric adenocarcinoma and MALT lymphoma. Its virulence is essentially mediated by CagA, injected into cells of the gastric mucosa. Thanks to high throughput sequencing of miRNA content of a gastric epithelial cell line, infected or not with H. pylori: miR-200b and -200c appeared up-regulated upon infection. These miRNA are potent inhibitors of the “epithelial-to-mesenchymal transition” (EMT), a process that drastically alters cell morphology and promotes cell invasion. MiR-200b/c target the transcription factors ZEB1 and ZEB2, with which they are involved in a mutually repressive feedback loop. In basal conditions, the high levels miR-200b/c in gastric epithelial cells totally silence ZEB1 mRNA whereas H. pylori promotes EMT via ZEB1 expression, on the dependence of CagA translocation into host cells. But, paradoxically, miR-200b/c levels were also up-regulated upon infection. The increased miR-200b/c levels in infected cells moderate ZEB1 induction thanks to NF-kB activation and constitute a self-defense mechanism to thwart the loss of their epithelial phenotype upon infection
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/.
Full textEnroth, 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/.
Full textBartfeld, 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.
Full textInfection 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.
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/.
Full textPetersson, 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.
Full textNgoyi, Esther Nina. "Résistance de Helicobacter pylori aux antibiotiques et d’autres substances antimicrobiennes. : Aspects moléculaires des mécanismes de détection." Thesis, Bordeaux, 2016. http://www.theses.fr/2016BORD0442/document.
Full textContext: The objective of this work was to improve Helicobacter pylori infection management. Materials and methods: H. pylori detection, it’s resistance to clarithromycine, tetracyclin, levofloxacin, and determination pathogenic genes were done by real-time PCR on 23 S rRNA, on 16 S rRNA gene, classic PCR, sequencing. Evaluation of the resistant mutant stability to its sensitive isolate was carried out by competing them over a long period in culture on AGS gastric cells and whole sequencing genome. The evaluation of Ceiba pentandra extract effect on H. pylori was carried out by determining the minimum inhibitory concentration. Results: Prevalence of H. pylori infection: 75.52%, resistance to clarithromycin and tetracycline: 4.2% and 1.2%, levofloxacin resistance: 57%. CagA gene: 92.2%. Vac As1m1 gene: 82%. Lack of stability of the resistant mutant in a 3695 R/S pair of isolates (R/S ratio 0.1), at the 30 day of the co-culture (p <0.05); this mutant had an A2142G mutation conferring resistance to clarithromycin. Stability of the resistant mutant in the other 3657 pair of isolates (R/S ratio of 1.7) at the 40 day of the co-culture (p <0.05), with development of compensatory mutations; this mutant had an A2143G mutation conferring resistance to clarithromycin. The moderate to low activity was noted with the hydroethanol extract and the butanol extract: minimum inhibitory concentration: 50 to 80 μg / ml. Conclusion: It’s possible to treat H. pylori infection with therapy based on clarithromycin in Congo. The absence of a strong activity does not make it possible to recommend Ceiba pentandra in the treatment of H. pylori infection. Reversion resistance is possible with H. pylori
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.
Full textNotre 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
info:eu-repo/semantics/nonPublished
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.
Full textMicroRNAs, 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
Olive, Claude. "Séroépidémiologie de l'infection à hélicobacter pylori dans l'ile de la Réunion." Bordeaux 2, 1991. http://www.theses.fr/1991BOR23028.
Full textNayak, 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.
Find full textThévenot, Sarah. "Variations génétiques chez Helicobacter pylori au cours d'une infection expérimentale murine : rôle de la polyphosphate kinase dans la colonisation." Poitiers, 2002. http://www.theses.fr/2002POIT1802.
Full textAudibert, Céline. "Polymorphisme des régions génomiques liées à la virulence chez Helicobacter pylori." Poitiers, 2000. http://www.theses.fr/2000POIT1805.
Full textMasso, 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.
Full textDissertation (MSc)--University of Pretoria 2020.
National Research Foundation Student bursary
Pharmacology
MSc (Pharmacology)
Unrestricted
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.
Full textBlancan, 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.
Full textEngberg, 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.
Full textFall, Katja. "Medical interventions and gastric cancer risk : an observational approach /." Stockholm, 2004. http://diss.kib.ki.se/2004/91-7349-905-6/.
Full textSevin, Eric. ""Helicobacter pylori" : sensibilité aux antibiotiques, identification et détection de la résistance à la clarithromycine par amplification génique." Paris 5, 1997. http://www.theses.fr/1997PA05P069.
Full textNeto, Cunha Gomes Joana. "Biological effects of Pteridium aquilinum and its toxin in gastric carcinogenesis : relationship with Helicobacter pylori infection." Thesis, Paris 11, 2012. http://www.theses.fr/2012PA114822.
Full textThe multifactorial gastric carcinogenesis process encompasses host genetic susceptibility, bacterial and environmental factors. Humans can directly consume or be indirectly exposed to toxic compounds present in plants, such as the bracken fern Pteridium aquilinum. This plant has a carcinogenic toxin, ptaquiloside, and is known to cause severe health problems in animals, including cancer. Epidemiological evidence also demonstrated an association between bracken exposure and gastric cancer development in Humans. Additionally, another major etiological agent is Helicobacter pylori, a bacterium that colonizes the stomach inducing a genotoxic response in gastric cells. This study aimed to characterize the biological and molecular involvement of Pteridium aquilinum and its ptaquiloside toxin in the gastric carcinogenesis process and to evaluate the potential synergistic effect of H. pylori infection.We observed that treatment with Pteridium aquilinum extracts and ptaquiloside toxin decreased cell viability and promoted cell apoptosis in gastric epithelial cells. A genotoxic effect with induction of DNA strand breaks was noted and it was exacerbated in the presence of H. pylori infection. We further demonstrated that in treated cells a p53 accumulation occurs, controlled by the activation of the ATR-Chk1 DNA damage signalling pathway. An increased level of p53 was also detected in the presence of a H. pylori virulent strain. The contribution of ptaquiloside to this genotoxic activity was supported by the deregulation of other genes involved in DNA cell cycle regulation and DNA repair. In addition, using a mouse model exposed to Pteridium aquilinum, we detected histomorphological alterations with increased cell proliferation and induction of frameshift events in the p53 gene. However, a concomitant chronic treatment with Pteridium aquilinum and H. pylori infection did not produce significant differences in p53 gene expression.Moreover, an altered glycophenotypic pattern was induced in the gastric mucosa of mice upon Pteridium aquilinum treatment in the presence of H. pylori infection. Several glycosyltransferases involved in the biosynthesis of simple mucin-type carbohydrate antigens and terminal Lewis antigens were differently expressed in the absence and presence of H. pylori, respectively. These results were also validated by an increased expression of Sialyl-LewisX.Further alterations in glycosyltransferases involved in the initial steps of O-glycosylation were observed. The ppGalNAcT6 was shown to have a heterogeneous expression in human gastric carcinoma, associated with the presence of venous invasion.Overall, our data supports the notion that cell exposure to the genotoxic and carcinogenic Pteridium aquilinum and ptaquiloside has a fundamental role in the promotion of gastric carcinogenesis. The synergistic environment associated to H. pylori infection underlines the importance of risk factor interplay in this process
A carcinogénese gástrica é um processo multifatorial que engloba fatores genéticos, bacterianos e ambientais. O Homem pode consumir diretamente ou ser exposto de forma indireta a compostos tóxicos presentes em plantas, como é o caso do feto vulgar Pteridium aquilinum. Esta planta tem uma toxina carcinogénica, o ptaquilosídeo, sendo conhecida a sua capacidade natural para induzir lesões neoplásicas em animais. Estudos epidemiológicos também demonstraram a existência de uma associação entre a exposição ao feto e o desenvolvimento de cancro gástrico em humanos. Outro fator etiológico importante é a Helicobacter pylori, uma bactéria que coloniza o estômago, induzindo nas células gástricas uma resposta genotóxica. Este estudo tem por objetivos caracterizar o envolvimento biológico e molecular do Pteridium aquilinum e da sua toxina, ptaquilosídeo, no processo de carcinogénese gástrica e avaliar o potencial efeito sinergístico da infeção por H. pylori.Observámos em células epiteliais gástricas que o tratamento com extratos de Pteridium aquilinum e com a toxina ptaquilosídeo, diminui a viabilidade celular e promove a apoptose. Foi demonstrado um efeito genotóxico com indução de quebras na cadeia de ADN, exacerbado pela presença da infeção por H. pylori. Demonstrámos ainda que, em células tratadas, ocorria uma acumulação de p53, controlada pela ativação da via de sinalização ATR-Chk1. Um aumento nos níveis de p53 foi igualmente detetado na presença de estirpes virulentas de H. pylori. A contribuição do ptaquilosídeo para esta atividade genotóxica foi também apoiada pela desregulação de outros genes envolvidos na regulação do ciclo celular e na reparação do ADN. Adicionalmente, usando um modelo de ratinho exposto ao Pteridium aquilinum, foram detetadas alterações histomorfológicas, bem como um aumento da proliferação celular e indução de mutações no gene p53. Contudo, um tratamento crónico com Pteridium aquilinum e infeção concomitante por H. pylori não produziu diferenças significativas na expressão do gene p53.Um padrão glicofenotípico alterado foi também observado na mucosa gástrica de ratinhos tratados com Pteridium aquilinum na presença de infeção por H. pylori. Várias glicosiltransferases envolvidas na biossíntese de antigénios simples das mucinas e antigénios terminais do tipo Lewis apresentaram uma expressão alterada, respetivamente, na ausência ou presença de H. pylori. Estes resultados foram também validados através de um aumento da expressão de Sialil-LewisX.Foram ainda observadas alterações em glicosiltransferases que estão envolvidas nas etapas iniciais de O-glicosilação. A ppGalNAcT6 apresentou uma expressão alterada em carcinomas gástricos, estando associada à presença de invasão venosa.No geral, estes dados suportam a evidência de que a exposição das células aos genotóxicos e carcinogénicos Pteridium aquilinum e ptaquilosídeo, tem um papel fundamental na promoção da carcinogénese gástrica. O ambiente sinergístico associado à infeção com H. pylori salienta a importância da interação entre os fatores de risco que dão origem a este processo