Relevant bibliographies by topics / Helicobacter hepaticus

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Academic literature on the topic 'Helicobacter hepaticus'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "Helicobacter hepaticus"

1

Hynes, Sean O., Susann Teneberg, Niamh Roche, and Torkel Wadström. "Glycoconjugate Binding of Gastric and Enterohepatic Helicobacter spp." Infection and Immunity 71, no. 5 (May 2003): 2976–80. http://dx.doi.org/10.1128/iai.71.5.2976-2980.2003.

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ABSTRACT Helicobacter pylori is able to utilize several lectin-like, protein-carbohydrate interactions for binding to mucins, cell surfaces, and extracellular matrix proteins. As determined by hemagglutination assays and binding of radiolabeled bacteria to glycosphingolipids on thin-layer chromatograms, strains of gastric helicobacters and enterohepatic helicobacters, including Helicobacter canis, Helicobacter hepaticus, and Helicobacter bilis, also demonstrated evidence for the presence of lectin-hemagglutinin adhesins. In addition, in H. hepaticus and H. bilis, binding may be sialic acid dependent. The presence or absence and differences in the levels of activity of lectin adhesins may reflect the species' ecological niche.
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Belzer, Clara, Jeroen Stoof, Catherine S. Beckwith, Ernst J. Kuipers, Johannes G. Kusters, and Arnoud H. M. van Vliet. "Differential regulation of urease activity in Helicobacter hepaticus and Helicobacter pylori." Microbiology 151, no. 12 (December 1, 2005): 3989–95. http://dx.doi.org/10.1099/mic.0.28188-0.

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Helicobacter hepaticus is a pathogen of rodents, which causes diverse enteric and hepatic inflammatory diseases and malignancies. The urease enzyme is an important colonization factor of gastric Helicobacter species like Helicobacter pylori, but little is known about the role and regulation of urease in enterohepatic Helicobacter species. Here it is reported that urease activity of H. hepaticus does not contribute to acid resistance, and that it is nickel-responsive at the post-translational level. H. hepaticus strain ATCC 51449 did not grow or survive at pH 3·0, and supplementation with urea or NiCl2 did not abrogate this acid sensitivity. Furthermore, urease enzyme activity of H. hepaticus was acid-independent, which contrasts with the acid-induced urease system of H. pylori. Nickel supplementation of Brucella medium resulted in a tenfold increase in urease activity in both H. hepaticus and H. pylori, but the maximum level of urease activity in H. hepaticus was still three- to fivefold lower when compared to H. pylori in the same conditions. The increase in urease activity of H. hepaticus was not associated with elevation of urease mRNA or protein levels. Inhibition of protein synthesis by chloramphenicol did not affect nickel-responsive induction of urease activity in H. hepaticus, and confirmed that nickel induction occurs at the post-translational level, probably by activation of preformed apo-enzyme. In conclusion, both the role of the urease enzyme and the regulation of urease activity differ between the enterohepatic pathogen H. hepaticus and the gastric pathogen H. pylori.
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Krishnan, Navasona, Alan R. Doster, Gerald E. Duhamel, and Donald F. Becker. "Characterization of a Helicobacter hepaticus putA Mutant Strain in Host Colonization and Oxidative Stress." Infection and Immunity 76, no. 7 (May 5, 2008): 3037–44. http://dx.doi.org/10.1128/iai.01737-07.

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ABSTRACT Helicobacter hepaticus is a gram-negative, spiral-shaped microaerophilic bacterium associated with chronic intestinal infection leading to hepatitis and colonic and hepatic carcinomas in susceptible strains of mice. In the closely related human pathogen Helicobacter pylori, l-proline is a preferred respiratory substrate and is found at significantly high levels in the gastric juice of infected patients. A previous study of the proline catabolic PutA flavoenzymes from H. pylori and H. hepaticus revealed that Helicobacter PutA generates reactive oxygen species during proline oxidation by transferring electrons from reduced flavin to molecular oxygen. We further explored the preference for proline as a respiratory substrate and the potential impact of proline metabolism on the redox environment in Helicobacter species during host infection by disrupting the putA gene in H. hepaticus. The resulting putA knockout mutant strain was characterized by oxidative stress analysis and mouse infection studies. The putA mutant strain of H. hepaticus exhibited increased proline levels and resistance to oxidative stress relative to that of the wild-type strain, consistent with proline's role as an antioxidant. The significant increase in stress resistance was attributed to higher proline content, as no upregulation of antioxidant genes was observed for the putA mutant strain. The wild-type and putA mutant H. hepaticus strains displayed similar levels of infection in mice, but in mice challenged with the putA mutant strain, significantly reduced inflammation was observed, suggesting a role for proline metabolism in H. hepaticus pathogenicity in vivo.
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Young, Vincent B., Kimberly A. Knox, and David B. Schauer. "Cytolethal Distending Toxin Sequence and Activity in the Enterohepatic Pathogen Helicobacter hepaticus." Infection and Immunity 68, no. 1 (January 1, 2000): 184–91. http://dx.doi.org/10.1128/iai.68.1.184-191.2000.

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ABSTRACT Little is known about the molecular pathogenesis of hepatitis and enterocolitis caused by enterohepatic Helicobacter species. Sonicates of the murine pathogen Helicobacter hepaticuswere found to cause progressive cell distension, accumulation of filamentous actin, and G2/M cell cycle arrest in HeLa cell monolayers. The genes encoding this cytotoxic activity were cloned fromH. hepaticus. Three open reading frames with closest homology to cdtA, cdtB, and cdtCfrom Campylobacter jejuni were identified. Sonicates of a laboratory strain of Escherichia coli carrying the clonedcdtABC gene cluster from H. hepaticusreproduced the cytotoxic activities seen with sonicates of H. hepaticus. Cytolethal distending toxin activity is a potential virulence determinant of H. hepaticus that may play a role in the pathogenesis of Helicobacter-associated hepatitis and enterocolitis.
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Whary, M. T., T. J. Morgan, C. A. Dangler, K. J. Gaudes, N. S. Taylor, and J. G. Fox. "Chronic Active Hepatitis Induced by Helicobacter hepaticus in the A/JCr Mouse Is Associated with a Th1 Cell-Mediated Immune Response." Infection and Immunity 66, no. 7 (July 1, 1998): 3142–48. http://dx.doi.org/10.1128/iai.66.7.3142-3148.1998.

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ABSTRACT Helicobacter hepaticus infection in A/JCr mice results in chronic active hepatitis characterized by perivascular, periportal, and parenchymal infiltrates of mononuclear and polymorphonuclear cells. This study examined the development of hepatitis and the immune response of A/JCr mice to H. hepaticus infection. The humoral and cell-mediated T helper immune response was profiled by measuring the postinfection (p.i.) antibody response in serum, feces, and bile and by the production of cytokines and proliferative responses by splenic mononuclear cells to H. hepaticusantigens. Secretory immunoglobulin A (IgA) and systemic IgG2a antibody developed by 4 weeks p.i. and persisted through 12 months. Splenocytes from infected mice proliferated and produced more gamma interferon (IFN-γ) than interleukin-4 (IL-4) or IL-5 when cultured with H. hepaticus outer membrane proteins. The predominantly IgG2a antibody response in serum and the in vitro production of IFN-γ in excess of IL-4 or IL-5 are consistent with a Th1 immune response reported in humans and mice infected withHelicobacter pylori and Helicobacter felis, respectively. Mice infected with H. hepaticus developed progressively severe perivascular, periportal, and hepatic parenchymal lesions consisting of lymphohistiocytic and plasmacytic cellular infiltrates. In addition, transmural typhlitis was observed at 12 months p.i. The characterization of a cell-mediated Th1 immune response toH. hepaticus infection in the A/JCr mouse should prove valuable as a model for experimental regimens which manipulate the host response to Helicobacter.
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Shen, Zeli, David B. Schauer, Harry L. T. Mobley, and James G. Fox. "Development of a PCR-Restriction Fragment Length Polymorphism Assay Using the Nucleotide Sequence of the Helicobacter hepaticus Urease Structural Genes ureAB." Journal of Clinical Microbiology 36, no. 9 (1998): 2447–53. http://dx.doi.org/10.1128/jcm.36.9.2447-2453.1998.

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Infection with Helicobacter hepaticus causes chronic active hepatitis in certain strains of mice and is associated with hepatocellular carcinoma in A/JCr mice. Like the gastric helicobacters,H. pylori and H. mustelae, H. hepaticus possesses a high level of urease activity. However, theH. hepaticus urease structural gene sequences have not been previously determined, and the role of the urease enzyme in colonization and in pathogenesis is not known. PCR was used to amplify a portion of the urease structural genes from H. hepaticusgenomic DNA. Amplified DNA fragments were cloned, and the nucleotide sequence was determined. The deduced amino acid sequence of the partialH. hepaticus ureA gene product was found to exhibit 60% identity and 75% similarity to the predicted H. pyloriUreA. The deduced amino acid sequence of a partial H. hepaticus ureB gene product exhibited 75% identity and 87% similarity to the predicted H. pylori UreB. Diversity amongH. hepaticus isolates was evaluated by means of a restriction fragment length polymorphism (RFLP) assay. The 1.6-kb fragments within the ureAB open reading frames, amplified from 11 independent isolates, were digested with the restriction endonuclease HhaI. Three distinct RFLP patterns were observed. Identical RFLP profiles were noted in sequential isolates of one strain of H. hepaticus during an 18 month in vivo colonization study, suggesting that the urease genes ofH. hepaticus are stable. The urease genes amongH. hepaticus strains were also well conserved, showing 98.8 to 99% nucleotide sequence identity among three isolates analyzed. These findings indicate that H. hepaticus has urease structural genes which are homologous to those of the gastric Helicobacter species and that these gene sequences can be used in a PCR and RFLP assay for diagnosis of this important murine pathogen.
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García, Alexis, Melanie M. Ihrig, Rebecca C. Fry, Yan Feng, Sandy Xu, Samuel R. Boutin, Arlin B. Rogers, Suresh Muthupalani, Leona D. Samson, and James G. Fox. "Genetic Susceptibility to Chronic Hepatitis Is Inherited Codominantly in Helicobacter hepaticus-Infected AB6F1 and B6AF1 Hybrid Male Mice, and Progression to Hepatocellular Carcinoma Is Linked to Hepatic Expression of Lipogenic Genes and Immune Function-Associated Networks." Infection and Immunity 76, no. 5 (February 19, 2008): 1866–76. http://dx.doi.org/10.1128/iai.01044-07.

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ABSTRACT Helicobacter hepaticus causes hepatitis in susceptible strains of mice. Previous studies indicated that A/JCr mice are susceptible and C57BL/6NCr mice are resistant to H. hepaticus-induced hepatitis. We used F1 hybrid mice derived from A/J and C57BL/6 matings to investigate their phenotype and determine their hepatic gene expression profile in response to H. hepaticus infection. F1 hybrid mice, as well as parental A/J and C57BL/6 mice, were divided equally into control and H. hepaticus-infected groups and euthanized at 18 months postinoculation. Hepatic lesions were evaluated histologically and the differential hepatic gene expression in F1 mice was determined by microarray-based global gene expression profiling analysis. H. hepaticus-infected parental strains including A/J and C57BL/6 mice, as well as F1 mice, developed significant hepatitis. Overall, hepatocellular carcinomas or dysplastic liver lesions were observed in 69% of H. hepaticus-infected F1 male mice and H. hepaticus was isolated from hepatic tissues of all F1 mice with liver tumors. Liver tumors, characterized by hepatic steatosis, developed in livers with high hepatitis scores. To identify gene expression specific to H. hepaticus-induced hepatitis and progression to hepatocellular carcinoma in F1 mice, a method using comparative group transcriptome analysis was utilized. The canonical pathway most significantly enriched was immunological disease. Fatty acid synthase and steaoryl-coenzyme A desaturase, the two rate-limiting enzymes in lipogenesis, were upregulated in neoplastic relative to dysplastic livers. This study suggests a synergistic interaction between hepatic steatosis and infectious hepatitis leading to hepatocellular carcinoma. The use of AB6F1 and B6AF1 mice, as well as genetically engineered mice, on a C57BL/6 background will allow studies investigating the role of chronic microbial hepatitis and steatohepatitis in the pathogenesis of liver cancer.
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Péré-Védrenne, Christelle, Wencan He, Lamia Azzi-Martin, Valérie Prouzet-Mauléon, Alice Buissonnière, Bruno Cardinaud, Philippe Lehours, Francis Mégraud, Christophe F. Grosset, and Armelle Ménard. "The Nuclear Remodeling Induced by Helicobacter Cytolethal Distending Toxin Involves MAFB Oncoprotein." Toxins 12, no. 3 (March 12, 2020): 174. http://dx.doi.org/10.3390/toxins12030174.

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Enterohepatic Helicobacters, such as Helicobacter hepaticus and Helicobacter pullorum, are associated with several intestinal and hepatic diseases. Their main virulence factor is the cytolethal distending toxin (CDT). In the present study, whole genome microarray-based identification of differentially expressed genes was performed in vitro in HT-29 intestinal cells while following the ectopic expression of the active CdtB subunit of H. hepaticus CDT. A CdtB-dependent upregulation of the V-maf musculoaponeurotic fibrosarcoma oncogene homolog B (MAFB) gene encoding the MAFB oncoprotein was found, as well as the CdtB-dependent regulation of several MAFB target genes. The transduction and coculture experiments confirmed MAFB mRNA and protein induction in response to CDT and its CdtB subunit in intestinal and hepatic cell lines. An analysis of MAFB protein subcellular localization revealed a strong nuclear and perinuclear localization in the CdtB-distended nuclei in intestinal and hepatic cells. MAFB was also detected at the cell periphery of the CdtB-induced lamellipodia in some cells. The silencing of MAFB changed the cellular response to CDT with the formation of narrower lamellipodia, a reduction of the increase in nucleus size, and the formation of less γH2AX foci, the biomarker for DNA double-strand breaks. Taken together, these data show that the CDT of enterohepatic Helicobacters modulates the expression of the MAFB oncoprotein, which is translocated in the nucleus and is associated with the remodeling of the nuclei and actin cytoskeleton.
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Ananieva, Olga, Ingrid Nilsson, Tamara Vorobjova, Raivo Uibo, and Torkel Wadström. "Immune Responses to Bile-Tolerant Helicobacter Species in Patients with Chronic Liver Diseases, a Randomized Population Group, and Healthy Blood Donors." Clinical and Vaccine Immunology 9, no. 6 (November 2002): 1160–64. http://dx.doi.org/10.1128/cdli.9.6.1160-1164.2002.

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ABSTRACT Bile-tolerant Helicobacter species such as Helicobacter pullorum, Helicobacter bilis, and Helicobacter hepaticus are associated with hepatic disorders in animals and may be involved in the pathogenesis of chronic liver diseases (CLD) in humans. Antibody responses to cell surface proteins of H. pullorum, H. bilis, and H. hepaticus in serum samples from patients with CLD, a randomized population group, and healthy blood donors were evaluated by using enzyme linked immunosorbent assay (ELISA). The results were compared with the antibody responses to Helicobacter pylori. For analysis of a possible cross-reactivity between bile-tolerant Helicobacter species and H. pylori, sera from a subpopulation of each group were absorbed with a whole-cell extract of H. pylori and retested by ELISA. Results before absorption showed that the mean value of the ELISA units for H. pullorum was significantly higher in patients with CLD than in healthy blood donors (P = 0.01). Antibody reactivity to cell surface protein of H. hepaticus was also significantly higher in the CLD patients than in the healthy blood donors and the population group (P = 0.005 and P = 0.002, respectively). Following the absorption, antibody responses to H. pullorum decreased significantly in all three groups (P = 0.0001 for CLD patients, P = 0.0005 for the population group, and P < 0.0001 for the blood donors), indicating that cross-reactivity between H. pylori and other Helicobacter spp. occurs. The antibody responses to H. hepaticus and H. bilis in CLD patients remained high following absorption experiments compared to ELISA results before absorption. The significance of this finding requires further investigations.
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Livingston, Robert S., Lela K. Riley, Reuel R. Hook, Cynthia L. Besch-Williford, and Craig L. Franklin. "Cloning and Expression of an Immunogenic Membrane-Associated Protein of Helicobacter hepaticus for Use in an Enzyme-Linked Immunosorbent Assay." Clinical Diagnostic Laboratory Immunology 6, no. 5 (September 1, 1999): 745–50. http://dx.doi.org/10.1128/cdli.6.5.745-750.1999.

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ABSTRACT Helicobacter hepaticus is a bacterial pathogen that causes chronic active hepatitis and inflammatory bowel disease in mice. The purpose of this study was to develop a recombinant antigen-based enzyme-linked immunosorbent assay (ELISA) to detect H. hepaticus-infected mice. A genomic library of H. hepaticus was constructed and was screened with sera fromH. hepaticus-infected mice. A 459-bp open reading frame that coded for an 18-kDa immunoreactive protein, MAP18, was identified. The gene had high identity with genes coding for outer membrane proteins of other bacteria, and the predicted amino acid sequence of MAP18 had a putative membrane-trafficking signal sequence and a putative signal peptidase II cleavage site. The recombinant protein was expressed in Escherichia coli as a glutathioneS-transferase (GST) fusion protein, GST-MAP18, and purified by affinity chromatography. The 44-kDa fusion protein was detected on Western blots probed with sera from H. hepaticus-infected mice but was not detected on blots probed with sera from mice infected with Helicobacter muridarum or Helicobacter bilis or with sera from mice free of Helicobacterinfection. The GST-MAP18 fusion protein was used as an antigen in an ELISA to detect anti-H. hepaticus antibodies in sera from infected mice. This ELISA was compared to an H. hepaticus-specific ELISA that uses a detergent extract ofH. hepaticus as the antigen. Sera from mice naturally and experimentally infected with H. hepaticus, H. bilis, or H. muridarum and sera from mice free ofHelicobacter infection were evaluated. Both ELISAs performed with a high specificity (98%); however, the detergent extract-based ELISA performed with a higher sensitivity (89%) than the recombinant protein-based ELISA (sensitivity, 66%). These data indicate that H. hepaticus carries a gene that encodes an immunogenic 18-kDa membrane-associated protein; however, antibodies to this protein are not detected in all infected mice.
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Dissertations / Theses on the topic "Helicobacter hepaticus"

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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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Lefevre, Marie. "Role of Helicobacter hepaticus in intestinal inflammation." Thesis, University of Oxford, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.504422.

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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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McBee, Megan Earley. "Immunomodulation by subclinical persistent infection with Helicobacter hepaticus." Thesis, Massachusetts Institute of Technology, 2007. http://hdl.handle.net/1721.1/39916.

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Thesis (Ph. D.)--Massachusetts Institute of Technology, Biological Engineering Division, 2007.
Includes bibliographical references (leaves 112-118).
Recognition of polymicrobial infections is becoming important for understanding differential host responses to environmental exposures, vaccines, as well as therapeutics. Citrobacter rodentium is a well-characterized model of infectious colitis with particular usefulness for modeling human diarrheal disease or inflammatory bowel disease. Infection with Helicobacter hepaticus is subclinical and persistent in C57BL/6 mice, but causes disease in susceptible strains and immunodeficient mice. To test the hypothesis that subclinical persistent infection modulates the host response to diarrheal disease a polymicrobial mouse model utilizing H. hepaticus and C. rodentium was developed and characterized. Concurrent infection has been shown to modulate disease outcome through several mechanisms including: cross-reactivity between viral antigens; shifting T cell response from Th1 to Th2 by helminth infection; and induction of regulatory T cells that suppress host response. In this new model of polymicrobial infection, a new paradigm in which persistent infection prolonged the course of acute colitis associated with a deviation from Thl-biased disease to Th17 was observed.
(cont.) In addition, Foxp3+naturally-occurring regulatory T cells (nTre,) were markedly increased during active colitis. The accumulation of nTreg was sustained when mice were persistently infected with H. hepaticus, indicating on-going active colitis. Although persistent infection was able to modulate host response, protective immunity to a subsequent C. rodentium infection was not compromised. Persistent infection also modulated host response to soluble antigen by preventing induction of oral tolerance to single bolus, but not to continuous, high-dose antigen feeding. Using H. hepaticus infection of C57BL/6 mice, models to investigate the immunomodulatory potential of persistent infection on immunogenic responses of protective immunity to enteric infection, host response to polymicrobial enteric infection, as well as tolerogenic responses to soluble antigen were developed. These models establish baselines for further investigation into the influences of persistent infection on host immune responses.
by Megan Earley McBee.
Ph.D.
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Boutin, Samuel R. 1952. "Molecular pathogenesis of Helicobacter hepaticus induced liver disease." Thesis, Massachusetts Institute of Technology, 2005. http://hdl.handle.net/1721.1/35696.

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Thesis (Ph. D. in Molecular and Systems Bacterial Pathogenesis)--Massachusetts Institute of Technology, Biological Engineering Division, 2005.
This electronic version was submitted by the student author. The certified thesis is available in the Institute Archives and Special Collections.
Includes bibliographical references.
Helicobacter hepaticus infection of A/JCr mice is a model of liver cancer resulting from chronic active inflammation. We monitored hepatic global gene expression profiles and correlated them to histological liver lesions in H. hepaticus infected and control male A/JCr mice at 3 months, 6 months, and 1 year of age. We used an Affymetrix-based oligonucleotide microarray platform on the premise that a specific genetic expression signature at isolated time points would be indicative of disease status. Model based expression index comparisons generated by dChip yielded consistent profiles of differential gene expression for H. hepaticus infected male mice with progressive liver disease versus uninfected control mice within each age group. Linear discriminant analysis and principal component analysis allowed segregation of mice based on combined age and lesion status, or age alone. Up-regulated genes present throughout the 12 month study involved inflammation, tissue repair, and host immune function. Upregulation of putative tumor and proliferation markers correlated with advancing hepatocellular dysplasia. Transcriptionally down-regulated genes in mice with liver lesions included those related to peroxisome proliferator, cholesterol, and steroid metabolism pathways. Transcriptional profiling of hepatic genes documented gene expression signatures in the livers of H. hepaticus infected male A/JCr mice with chronic progressive hepatitis and preneoplastic liver lesions, complemented the histopathological diagnosis, and suggested molecular targets for the monitoring and intervention of disease progression prior to the onset of hepatocellular neoplasia. Our laboratory, in collaboration with Professors Suerbaum and Schauer, recently identified a
(cont.) 70kb genomic island in Helicobacter hepaticus strain ATCC 51488 as a putative pathogenicity island (HhPAI) (Suerbaum et al, PNAS, 2003). This region within H. hepaticus contains genes HH0233-HH0302, a differential GC content, several long tandem repeats but no flanking repeats, and three components of a type IV secretion system (T4SS). A/JCr mice were experimentally infected with three naturally occurring strains of H. hepaticus including the type strain H. hepaticus ATCC 51488 strain (Hh 3B1) isolated from A/JCr mice, MIT 96-1809 (Hh NET) isolated from mice shipped from the Netherlands, and MIT-96-284 (HhG) isolated from mice acquired from Germany.4 HhNET (missing most of the HhPAI) infected male A/JCR mice exhibited a significantly lower prevalence (p<.05) of hepatic lesions at 6 months post infection than Hh 3B1 with an intact HhPAI. Hh G also has a large segment of the genomic island deleted, but not as many genes are deleted as compared to Hh NET. Hh G also demonstrated a lower prevalence of hepatic lesions. This variable pathological effect was evident in male mice only. The severity of chronic active inflammation in the liver of the H. hepaticus infected A/JCr mice depended on H. hepaticus liver colonization levels. The in vivo results support the presence of the HhPAI as a legitimate virulence determinant and predictor of severity of liver lesions in H. hepaticus infected A/JCr male mice. To further determine the differences in virulence of the H. hepaticus strains Hh 3B1, Hh NET, Hh G and an isogenic mutant H. ...
by Samuel R. Boutin.
Ph.D.in Molecular and Systems Bacterial Pathogenesis
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Avenaud, Philippe. "Hélicobacters et carcinomes hépatocelluaires : recherche de bactéries du genre Helicobacter dans le foie humain et de souris par méthode moléculaire." Bordeaux 2, 2003. http://www.theses.fr/2003BOR21067.

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Belzer, Clara. "Surviving the Enterohepatic Tract: Molecular Mechanisms of Stress Adaptation in Helicobacter hepaticus." [S.l.] : Rotterdam : [The Author] ; Erasmus University [Host], 2007. http://hdl.handle.net/1765/10647.

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Okoli, Arinze Stanley Medical Sciences Faculty of Medicine UNSW. "Molecular studies of the response of Helicobacter hepaticus to bile, and the effect of Helicobacter bilis on human hepatoma cells." Publisher:University of New South Wales. Medical Sciences, 2009. http://handle.unsw.edu.au/1959.4/43379.

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Enterohepatic Helicobacter species (EHS) are emerging infectious disease agents. Infection of the enterohepatobiliary tract of several mammals by this group of bacteria results in various pathological disorders. The availability of the Helicobacter hepaticus sequenced and annotated genome, allowed molecular characterisation of the responses of H. hepaticus to host factors such as bile. The adaptation/responses of the bacterium to bovine, porcine and human bile were investigated using proteomics and transcriptomics. Ninety-one different proteins were identified in the responses of H. hepaticus response to the three types of bile. These proteins participate in several key cellular processes including DNA replication; protein transcription, translation and folding; oxidative stress response; motility; virulence; and metabolism. In particular, the bacteria deployed several strategies such as inhibition of the TCA cycle and the electron transport chain as well as iron sequestration to ensure control of the levels of hydroxyl radicals. The results of this study revealed also the modulation by bile of the expression of H. hepaticus genes involved in response to oxidative stress and virulence. The responses of human HEp-2 and Huh7-derived cell-lines to H. hepaticus and Helicobacter bilis, respectively, were investigated employing proteomics and transcriptomics. One-hundred and twenty different proteins were differentially expressed in the responses of the human cells to the presence of Helicobacter spp. in the cell cultures. These proteins are involved in regulation of cell proliferation and structure; metabolism; protein transcription, translation and modification; stress response; and tumour induction. For example, in co-cultures of Huh7-derived cells and H. bilis, the activation of several mitochondrial and endoplasmic reticulum stress-related proteins and the dysregulation of several apoptosis effectors were suggested as mechanisms that could result in the death of the liver cells. Importantly, the differential expression of several tumour-related proteins by the Huh7 cells supported a possible role for Helicobacter spp. in liver cancer.
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Evans, Stephanie. "A computational approach to studying the processes active during Helicobacter hepaticus-induced intestinal inflammation." Thesis, University of York, 2016. http://etheses.whiterose.ac.uk/16125/.

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Inflammatory bowel disease (IBD) is a chronic inflammatory condition of the gastro-intestinal tract that usually manifests as either ulcerative colitis or Crohn's disease. Helicobacter hepaticus (Hh)-induced colitis is a mouse model of intestinal inflammation whereby IL-10 knock out mice are infected with Hh, resulting in pathology similar to that seen in Crohn's disease. Following the Complex Systems Modelling and Simulation (CoSMoS) process, a principled approach to the engineering of simulations of complex systems, we have developed IBDSim, a computational model of the processes active in the intestinal tract during Hh-induced colitis. IBDSim is a hybrid agent-based model (ABM) that combines agent-based modelling with systems biology and quantitative systems pharmacology approaches, to capture both cell- and system-level behaviours. In combining these approaches, the Automated Simulation Parameter Alteration and SensItivity Analysis toolkit (ASPASIA) was developed to aid in the calibration and analysis of models written in Systems Biology Mark-up Language (SBML), where the addition of an intervention is required for key behaviours to emerge. SBML models generated using this toolkit could then be incorporated into IBDSim.
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Kamdar, Shraddha Rashmi. "Profiling of microRNAs and IL-10 expression in intestinal CD4+ T cells following infection with Helicobacter hepaticus." Thesis, University of York, 2015. http://etheses.whiterose.ac.uk/12188/.

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In the Helicobacter hepaticus (Hh) colitis model, Hh infection of either wild-type mice treated with a blocking antibody to the IL-10 receptor (anti-IL-10R) or IL-10 KO mice results in intestinal inflammation associated with inflammatory Th1 and Th17 responses. Recent findings suggest that altered expression of the post-transcriptional gene regulators microRNAs contribute to pathogenic immune responses during intestinal inflammation. Here, examination of microRNA expression during Hh colitis showed that microRNAs are differentially expressed in the inflamed large intestine of Hh+ IL-10 KO mice compared to uninfected controls, both at the tissue-level and the CD4+ T-cell level. Kinetic examination of the cecal and colonic levels of miR-155, miR-326 and miR-132 (microRNAs previously shown to augment Th1 and/or Th17 responses) demonstrated that miR-155 was up-regulated and miR-326 and miR-132 were down-regulated at different time points post Hh infection. Furthermore, the change in expression of these microRNAs coincided with inflammation development. Microarray profiling of large intestine LP CD4+ T cells revealed that two microRNAs were significantly up-regulated (miR-21a and miR-31) and seven microRNAs were significantly down-regulated (miR-125a, miR-125b, miR-139, miR-181a, miR-192, miR-30a and miR-467c) in colitic IL-10 KO mice compared to uninfected controls. The anti-inflammatory cytokine IL-10 is necessary for protection against intestinal inflammation. Here, the phenotype of IL-10-producing LP CD4+ T cells was examined in a non-inflammatory immune response (Hh+ WT mice) and in an inflammatory immune response (Hh+/anti-IL-10R-treated WT mice). Compared to uninfected controls, the Hh+ mice showed a slight expansion in IL-10+ IL-17A+FoxP3+/- cells whereas the Hh+/anti-IL-10R-treated mice showed a significant expansion in all the IL-10+ LP CD4+ T cells co-expressed both inflammatory cytokines IL-17A and/or IFN-γ and/or the Treg transcription factor FoxP3. The experiments carried out in this thesis demonstrate that the profile of two important regulatory factors, microRNAs and IL-10, is markedly different in LP CD4+ T cells from the colitic setting compared to uninfected controls.
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Books on the topic "Helicobacter hepaticus"

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Keshav, Satish, and Alexandra Kent. Gastrointestinal infections. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0197.

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Gastrointestinal infections include diarrhoeal diseases that are major causes of morbidity and mortality worldwide; viral hepatitis; and infections such as Helicobacter pylori infection in the stomach, and intestinal tuberculosis. Here, only luminal gastrointestinal infections causing gastroenteritis, manifested by diarrhoea and/or vomiting, are considered.
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Bulterys, Marc, Julia Brotherton, and Ding-Shinn Chen. Prevention of Infection-Related Cancers. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780190238667.003.0066.

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This chapter discusses primary prevention measures that disrupt transmission of oncogenic infections. It begins by discussing vaccination against hepatitis B virus (HBV) and human papillomavirus (HPV), two major causes of cancer for which safe and effective vaccines are currently available. It briefly discusses the importance of treatment and prophylaxis against human immunodeficiency virus type 1 (HIV-1), which potentiates the virulence of other viral infections as well as directly increasing the incidence of non-Hodgkin lymphoma. It does not discuss the treatment of HBV or hepatitis C virus (HCV) infection, since these are considered in Chapters 25 and 33. Also beyond the scope of this chapter are the randomized clinical trials currently underway to assess the efficacy and feasibility of eradication of Helicobacter pylori (Chapters 24, 31), vaccination against Epstein-Barr virus (EBV) (Chapters 24, 26, 39), or the prevention of schistosomiasis and liver flukes (Chapters 24, 33, and 52).
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Franceschi, Silvia, Hashem B. El-Serag, David Forman, Robert Newton, and Martyn Plummer. Infectious Agents. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780190238667.003.0024.

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Eleven infectious agents (seven viruses, three parasites, and one bacterium) have been classified by the International Agency for Research on Cancer as carcinogenic to humans for one or more cancer sites: hepatitis B virus; hepatitis C virus; thirteen types of human papillomavirus (HPV); human immunodeficiency virus type 1 (HIV-1); human T-cell leukemia virus type 1; Epstein-Barr virus; Kaposi sarcoma herpesvirus; Helicobacter pylori; Opisthorchis viverrini; Clonorchis sinensis; and Schistosoma haematobium. Other infectious agents, such as Merkel cell polyomavirus, Plasmodium falciparum, and cutaneous HPVs, have been classified as “probably carcinogenic” or “possibly carcinogenic.” Accurate biomarkers of chronic infection have been essential for estimating risk and ascribing a causal role to infectious agents in cancer. Of the 14 million cases of cancer estimated to have occurred worldwide in 2012, 2.2 million were caused by infectious agents. Vaccination and screen-and-treat programs have the potential for greatly reducing the burden of cancer caused by infections.
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Book chapters on the topic "Helicobacter hepaticus"

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Fox, J. G. "Helicobacter hepaticus and Helicobacter bilis: proinflammatory modulators of enterohepatic disease." In Helicobactor pylori, 15–29. Dordrecht: Springer Netherlands, 2003. http://dx.doi.org/10.1007/978-94-017-1763-2_2.

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Fox, J. G., K. A. Andrutis, and J. Yu. "Animal models for Helicobacter-induced gastric and hepatic cancer." In Helicobacter pylori, 504–22. Dordrecht: Springer Netherlands, 1994. http://dx.doi.org/10.1007/978-94-011-1418-9_49.

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Burnens, André P., John Stanley, and Jacques Nicolet. "Possible Association of Helicobacter pullorum with Lesions of Vibrionic Hepatitis in Poultry." In Campylobacters, Helicobacters, and Related Organisms, 291–93. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4757-9558-5_51.

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4

Simon, Chantal, Hazel Everitt, Françoise van Dorp, Nazia Hussain, Emma Nash, and Danielle Peet. "Gastrointestinal medicine." In Oxford Handbook of General Practice, 343–406. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198808183.003.0012.

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This chapter in the Oxford Handbook of General Practice explores gastrointestinal medicine in general practice. It covers assessment of abdominal pain, vomiting and diarrhoea, gastroenteritis and food poisoning, constipation, and other abdominal symptoms and signs. It examines dyspepsia and Helicobacter pylori, oesophageal conditions, gastro-oesophageal reflux and gastritis, peptic ulceration, and gastro-oesophageal malignancy. It discusses hernias, appendicitis and small bowel disease, colorectal cancer, and other large bowel conditions. It describes anal and perianal conditions, patients with ostomies, malabsorption, faecal incontinence, coeliac disease, inflammatory bowel disease, and irritable bowel syndrome. It also explores jaundice and abnormal liver function, fatty liver disease, hepatitis, liver failure and portal hypertension, gallbladder disease, pancreatitis, and pancreatic tumours.
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Conference papers on the topic "Helicobacter hepaticus"

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Gong, Guanyu, Sureshkumar Muthupalani, Gerald N. Wogan, James G. Fox, and Steven R. Tannenbaum. "Abstract A17: Colitis-associated tumorigenesis in the Rag2 -/- Helicobacter hepaticus-infected mouse features DNA damage and Retinoblastoma-mediated cell proliferation via nitric oxide but not hypochlorous acid." In Abstracts: Third AACR International Conference on Frontiers in Basic Cancer Research - September 18-22, 2013; National Harbor, MD. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.fbcr13-a17.

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