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Journal articles on the topic 'Helicobacter hepaticus'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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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 dep

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2

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

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3

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 b

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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 clu

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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 im

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6

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 nucleot

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7

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 histolog

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8

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

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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

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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

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Dvorak, Katerina, Christine F. Coursodon-Boyiddle, Chelsea L. Snarrenberg, Anchasa Kananurak, Mark A. Underwood, and Bohuslav Dvorak. "Helicobacter hepaticusincreases intestinal injury in a rat model of necrotizing enterocolitis." American Journal of Physiology-Gastrointestinal and Liver Physiology 305, no. 8 (October 15, 2013): G585—G592. http://dx.doi.org/10.1152/ajpgi.00483.2012.

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Enterohepatic helicobacter species (EHS) infect the intestinal tract and biliary tree, triggering intestinal and hepatic disorders. Helicobacter hepaticus, the prototypic murine EHS, is also associated with inflammation. Necrotizing enterocolitis (NEC) is a devastating disease of premature infants. The cause of NEC is not fully understood, but anomalies of bacterial colonization (dysbiosis) are thought to play an important role in disease onset. To evaluate the effect of H. hepaticus infection on the development of NEC, premature formula-fed rats were kept either in H. hepaticus-free condition

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12

Boutin, Samuel R., Zeli Shen, Arlin B. Rogers, Yan Feng, Zhongming Ge, Sandy Xu, Torsten Sterzenbach, et al. "Different Helicobacter hepaticus Strains with Variable Genomic Content Induce Various Degrees of Hepatitis." Infection and Immunity 73, no. 12 (December 2005): 8449–52. http://dx.doi.org/10.1128/iai.73.12.8449-8452.2005.

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ABSTRACT A 70-kb genomic island (HHGI1) in Helicobacter hepaticus strain ATCC 51449 is a putative pathogenicity island (PAI). To determine the in vivo relevance of this PAI, we inoculated A/JCr mice with one of three strains of H. hepaticus: type strain Hh3B1, which contains the complete PAI, and strains HhNET and HhG, which lack all or large parts of HHGI1, respectively. Mice infected with HhG and HhNET developed less-severe hepatitis than male A/JCr mice infected with Hh3B1.

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13

Beckwith, Catherine S., David J. McGee, Harry L. T. Mobley, and Lela K. Riley. "Cloning, Expression, and Catalytic Activity ofHelicobacter hepaticus Urease." Infection and Immunity 69, no. 9 (September 1, 2001): 5914–20. http://dx.doi.org/10.1128/iai.69.9.5914-5920.2001.

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ABSTRACT Helicobacter hepaticus causes disease in the liver and lower intestinal tract of mice. It is strongly urease positive, although it does not live in an acidic environment. The H. hepaticus urease gene cluster was expressed in Escherichia coli with and without coexpression of the Helicobacter pylori nickel transporter NixA. As for H. pylori, it was difficult to obtain enzymatic activity from recombinant H. hepaticus urease; special conditions including NiCl2supplementation were required. The H. hepaticus urease cluster contains a homolog of each gene in the H. pyloriurease cluster, incl

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14

Hong, Yang, Ge Wang, and Robert J. Maier. "A Helicobacter hepaticus catalase mutant is hypersensitive to oxidative stress and suffers increased DNA damage." Journal of Medical Microbiology 56, no. 4 (April 1, 2007): 557–62. http://dx.doi.org/10.1099/jmm.0.46891-0.

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Catalase (KatA) is known to play an important role in oxidative stress resistance in many bacterial species and a homologue exists in Helicobacter hepaticus, a member of the enterohepatic Helicobacter species. Here, a katA mutant was constructed by insertional mutagenesis and its oxidative stress phenotype was investigated. Catalase activity was readily detected [196 units (mg protein crude cell extract)−1] in the wild-type, whereas the mutant strain was deficient in, but not devoid of, activity. In contrast, Helicobacter pylori katA strains lack detectable catalase activity and wild-type H. p

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Dieleman, Levinus A., Annemarie Arends, Susan L. Tonkonogy, Marije S. Goerres, David W. Craft, Wetonia Grenther, Rance K. Sellon, Ed Balish, and R. Balfour Sartor. "Helicobacter hepaticus Does Not Induce or Potentiate Colitis in Interleukin-10-Deficient Mice." Infection and Immunity 68, no. 9 (September 1, 2000): 5107–13. http://dx.doi.org/10.1128/iai.68.9.5107-5113.2000.

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ABSTRACT Helicobacter hepaticus has been reported to induce colitis, hepatitis, and hepatocellular carcinoma in several different murine models. The aim of this study was to determine if H. hepaticus will cause colitis in monoassociated mice lacking the interleukin-10 gene (IL-10−/− mice) and potentiate colitis in specific-pathogen-free (SPF) IL-10−/− mice. Germfree IL-10−/− mice on either a mixed (C57BL/6 × 129/Ola) or inbred (129/SvEv) genetic background were monoassociated with H. hepaticus ATCC 51448 by oral feeding and rectal enemas. In a second experiment, germfree IL-10−/− mice were col

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16

Ge, Zhongming, Yan Feng, Mark T. Whary, Prashant R. Nambiar, Shilu Xu, Vivian Ng, Nancy S. Taylor, and James G. Fox. "Cytolethal Distending Toxin Is Essential for Helicobacter hepaticus Colonization in Outbred Swiss Webster Mice." Infection and Immunity 73, no. 6 (June 2005): 3559–67. http://dx.doi.org/10.1128/iai.73.6.3559-3567.2005.

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ABSTRACT Helicobacter hepaticus, which induces chronic hepatitis and typhlocolitis in susceptible mouse strains, produces a cytolethal distending toxin (CDT) consisting of CdtA, CdtB, and CdtC. A cdtB-deficient H. hepaticus isogenic mutant (HhcdtBm7) was generated and characterized for colonization parameters in four intestinal regions (jejunum, ileum, cecum, and colon) of outbred Swiss Webster (SW) mice. Inactivation of the cdtB gene abolished the ability of HhcdtBm7 to colonize female mice at both 8 and 16 weeks postinfection (wpi), whereas HhcdtBm7 colonized all of four intestinal regions o

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Sterzenbach, Torsten, Lucie Bartonickova, Wiebke Behrens, Birgit Brenneke, Jessika Schulze, Friederike Kops, Elaine Y. Chin, et al. "Role of the Helicobacter hepaticus Flagellar Sigma Factor FliA in Gene Regulation and Murine Colonization." Journal of Bacteriology 190, no. 19 (August 8, 2008): 6398–408. http://dx.doi.org/10.1128/jb.00626-08.

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ABSTRACT The enterohepatic Helicobacter species Helicobacter hepaticus colonizes the murine intestinal and hepatobiliary tract and is associated with chronic intestinal inflammation, gall stone formation, hepatitis, and hepatocellular carcinoma. Thus far, the role of H. hepaticus motility and flagella in intestinal colonization is unknown. In other, closely related bacteria, late flagellar genes are mainly regulated by the sigma factor FliA (σ28). We investigated the function of the H. hepaticus FliA in gene regulation, flagellar biosynthesis, motility, and murine colonization. Competitive mic

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Maier, Robert J., Jonathan Olson, and Adriana Olczak. "Hydrogen-Oxidizing Capabilities of Helicobacter hepaticus and In Vivo Availability of the Substrate." Journal of Bacteriology 185, no. 8 (April 15, 2003): 2680–82. http://dx.doi.org/10.1128/jb.185.8.2680-2682.2003.

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ABSTRACT Hydrogen-oxidizing hydrogenase activity was detected in Helicobacter hepaticus and compared to the activity in Helicobacter pylori for characteristics associated with hydrogen uptake respiratory hydrogenases. Intact whole cells could couple H2 oxidation to oxygen uptake, and no H2 uptake was observed without oxygen available to complete the respiratory pathway. The H. hepaticus enzyme coupled H2 oxidation to reduction of many positive potential acceptors, and it underwent anaerobic or reductive activation. H. hepaticus had a strong affinity for molecular H2 (apparent Km of 2.5 μM), an

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Pratt, Jason S., Kacey L. Sachen, Heather D. Wood, Kathryn A. Eaton, and Vincent B. Young. "Modulation of Host Immune Responses by the Cytolethal Distending Toxin of Helicobacter hepaticus." Infection and Immunity 74, no. 8 (August 2006): 4496–504. http://dx.doi.org/10.1128/iai.00503-06.

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ABSTRACT Persistent murine infection with Helicobacter hepaticus leads to chronic gastrointestinal inflammation and neoplasia in susceptible strains. To determine the role of the virulence factor cytolethal distending toxin (CDT) in the pathogenesis of this organism, interleukin-10-deficient (IL-10−/−) mice were experimentally infected with wild-type H. hepaticus and a CDT-deficient isogenic mutant. Both wild-type H. hepaticus and the CDT-deficient mutant successfully colonized IL-10−/− mice, and they reached similar tissue levels by 6 weeks after infection. Only animals infected with wild-typ

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Sterzenbach, Torsten, Sae Kyung Lee, Birgit Brenneke, Franz von Goetz, David B. Schauer, James G. Fox, Sebastian Suerbaum, and Christine Josenhans. "Inhibitory Effect of Enterohepatic Helicobacter hepaticus on Innate Immune Responses of Mouse Intestinal Epithelial Cells." Infection and Immunity 75, no. 6 (March 19, 2007): 2717–28. http://dx.doi.org/10.1128/iai.01935-06.

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ABSTRACT Enterohepatic Helicobacter species infect the intestinal tracts and biliary trees of various mammals, including mice and humans, and are associated with chronic inflammatory diseases of the intestine, gallstone formation, and malignant transformation. The recent analysis of the whole genome sequence of the mouse enterohepatic species Helicobacter hepaticus allowed us to perform a functional analysis of bacterial factors that may play a role in these diseases. We tested the hypothesis that H. hepaticus suppresses or evades innate immune responses of mouse intestinal epithelial cells, w

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Patterson, Mary M., Arlin B. Rogers, and James G. Fox. "Experimental Helicobacter marmotae infection in A/J mice causes enterohepatic disease." Journal of Medical Microbiology 59, no. 10 (October 1, 2010): 1235–41. http://dx.doi.org/10.1099/jmm.0.020479-0.

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Helicobacter marmotae has been identified in the inflamed livers of Eastern woodchucks (Marmota monax) infected with woodchuck hepatitis virus (WHV), as well as from the livers of WHV-negative woodchucks. Because the majority of WHV-positive woodchucks with hepatic tumours were culture or PCR positive for this helicobacter, and WHV-negative woodchucks with H. marmotae had hepatitis, the bacterium may have a role in tumour promotion related to chronic inflammation. In this study, the type strain of H. marmotae was inoculated intraperitoneally into 48 male and female A/J mice, a strain noted to

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Young, Vincent B., Kimberly A. Knox, Jason S. Pratt, Jennifer S. Cortez, Linda S. Mansfield, Arlin B. Rogers, James G. Fox, and David B. Schauer. "In Vitro and In Vivo Characterization of Helicobacter hepaticus Cytolethal Distending Toxin Mutants." Infection and Immunity 72, no. 5 (May 2004): 2521–27. http://dx.doi.org/10.1128/iai.72.5.2521-2527.2004.

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ABSTRACT Helicobacter hepaticus expresses a member of the cytolethal distending toxin (CDT) family of bacterial cytotoxins. To investigate the role of CDT in the pathogenesis of H. hepaticus, transposon mutagenesis was used to generate a series of isogenic mutants in and around the cdtABC gene cluster. An H. hepaticus transposon mutant with a disrupted cdtABC coding region no longer produced CDT activity. Conversely, a transposon insertion outside of the cluster did not affect the CDT activity. An examination of these mutants demonstrated that CDT represents the previously described granulatin

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Burich, Andrew, Robert Hershberg, Kim Waggie, Weiping Zeng, Thea Brabb, Gina Westrich, Joanne L. Viney, and Lillian Maggio-Price. "Helicobacter-induced inflammatory bowel disease in IL-10- and T cell-deficient mice." American Journal of Physiology-Gastrointestinal and Liver Physiology 281, no. 3 (September 1, 2001): G764—G778. http://dx.doi.org/10.1152/ajpgi.2001.281.3.g764.

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Inflammatory bowel disease (IBD) is thought to result from a dysregulated mucosal immune response to luminal microbial antigens, with T lymphocytes mediating the colonic pathology. Infection with Helicobacter spp has been reported to cause IBD in immunodeficient mice, some of which lack T lymphocytes. To further understand the role of T cells and microbial antigens in triggering IBD, we infected interleukin (IL)-10−/−, recombinase-activating gene (Rag)1−/−, T-cell receptor (TCR)-α−/−, TCR-β−/−, and wild-type mice with Helicobacter hepaticus or Helicobacter bilis and compared the histopathologi

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Avenaud, Philippe, Brigitte Le Bail, Kathryn Mayo, Armelle Marais, Rabia Fawaz, Paulette Bioulac-Sage, and Francis Megraud. "Natural History of Helicobacter hepaticus Infection in Conventional A/J Mice, with Special Reference to Liver Involvement." Infection and Immunity 71, no. 6 (June 2003): 3667–72. http://dx.doi.org/10.1128/iai.71.6.3667-3672.2003.

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ABSTRACT It has been reported that Helicobacter hepaticus infection of mice leads to chronic hepatitis and hepatocarcinoma. Our aim was to monitor a cohort of 80 conventional A/J mice in which half of the mice were infected by H. hepaticus in order to study the evolution of the infection and the pathological changes in comparison to uninfected mice. H. hepaticus was detected by culture only in some colon and cecum specimens after 17 months of age, while PCR detected H. hepaticus in the intestines of all inoculated mice after only 5 months of infection. The percentage of mice in which H. hepati

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Theve, Elizabeth J., Yan Feng, Koli Taghizadeh, Kathleen S. Cormier, David R. Bell, James G. Fox, and Arlin B. Rogers. "Sex Hormone Influence on Hepatitis in Young Male A/JCr Mice Infected with Helicobacter hepaticus." Infection and Immunity 76, no. 9 (June 16, 2008): 4071–78. http://dx.doi.org/10.1128/iai.00401-08.

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ABSTRACT Hepatitis B virus (HBV), the leading cause of human hepatocellular carcinoma, is especially virulent in males infected at an early age. Likewise, the murine liver carcinogen Helicobacter hepaticus is most pathogenic in male mice infected before puberty. We used this model to investigate the influence of male sex hormone signaling on infectious hepatitis. Male A/JCr mice were infected with H. hepaticus or vehicle at 4 weeks and randomized into surgical and pharmacologic treatment groups. Interruption of androgen pathways was confirmed by hormone measurements, histopathology, and liver

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Feng, Sunlian, Emir Hodzic, Lon V. Kendall, Amy Smith, Kimberly Freet, and Stephen W. Barthold. "Cloning and Expression of a Helicobacter bilis Immunoreactive Protein." Clinical and Vaccine Immunology 9, no. 3 (May 2002): 627–32. http://dx.doi.org/10.1128/cdli.9.3.627-632.2002.

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ABSTRACT In an effort to identify immunoreactive Helicobacter bilis antigens with potential for serodiagnosis, sera from mice experimentally infected with H. bilis were used to screen an H. bilis genomic DNA expression library. Among 17 immunoreactive clones, several contained sequences that encoded a predicted 167-kDa protein (P167). Five overlapping P167 peptides (P167A to P167E) of approximately 40 kDa each were generated and tested. Immune sera reacted with fragments P167C and P167D at dilutions of 1:1,600 and 1:6,400, respectively, and reacted with an H. bilis membrane extract at a diluti

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Nagamine, Claude M., Jane J. Sohn, Barry H. Rickman, Arlin B. Rogers, James G. Fox, and David B. Schauer. "Helicobacter hepaticus Infection Promotes Colon Tumorigenesis in the BALB/c-Rag2−/−ApcMin/+ Mouse." Infection and Immunity 76, no. 6 (April 14, 2008): 2758–66. http://dx.doi.org/10.1128/iai.01604-07.

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ABSTRACT Adenomatous polyposis coli (APC) mutations are linked to human and mouse colorectal cancers. The Apc multiple intestinal neoplasia (Min) mouse mutation causes adenomas to develop throughout the small and large intestines. The BALB-Min (C.B6-Apc Min/+) congenic strain was generated by backcrossing into BALB/c the Apc Min allele from C57BL/6J-Apc Min/+ mice. BALB-Min mice have a low tumor multiplicity (27.4 small intestine tumors/mouse) and a relatively long life span (>1 year) that makes them amenable to long-term studies. To investigate the interplay of the adaptive immune system a

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Peña, Jeremy A., Arlin B. Rogers, Zhongming Ge, Vivian Ng, Sandra Y. Li, James G. Fox, and James Versalovic. "Probiotic Lactobacillus spp. Diminish Helicobacter hepaticus-Induced Inflammatory Bowel Disease in Interleukin-10-Deficient Mice." Infection and Immunity 73, no. 2 (February 2005): 912–20. http://dx.doi.org/10.1128/iai.73.2.912-920.2005.

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ABSTRACT Clinical and experimental evidence has demonstrated the potential role of probiotics in the prevention or treatment of inflammatory bowel disease. Probiotic clones with direct immunomodulatory activity may have anti-inflammatory effects in the intestine. We investigated the roles of tumor necrosis factor alpha (TNF-α)-inhibitory Lactobacillus clones with a pathogen-induced murine colitis model. Murine-derived probiotic lactobacilli were selected in vitro for their ability to inhibit TNF-α secretion by Helicobacter hepaticus-stimulated macrophages. Interleukin-10 (IL-10)-deficient mice

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Kuehl, Carole J., Heather D. Wood, Terence L. Marsh, Thomas M. Schmidt, and Vincent B. Young. "Colonization of the Cecal Mucosa by Helicobacter hepaticus Impacts the Diversity of the Indigenous Microbiota." Infection and Immunity 73, no. 10 (October 2005): 6952–61. http://dx.doi.org/10.1128/iai.73.10.6852-6961.2005.

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ABSTRACT Establishment of mucosal and/or luminal colonization is the first step in the pathogenesis of many gastrointestinal bacterial pathogens. The pathogen must be able to establish itself in the face of competition from the complex microbial community that is already in place. We used culture-independent methods to monitor the colonization of the cecal mucosa of Helicobacter-free mice following experimental infection with the pathogen Helicobacter hepaticus. Two days after infection, H. hepaticus comprised a minor component of the mucosa-associated microbiota, but within 14 days, it became

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Fox, J. G., L. Yan, B. Shames, J. Campbell, J. C. Murphy, and X. Li. "Persistent hepatitis and enterocolitis in germfree mice infected with Helicobacter hepaticus." Infection and immunity 64, no. 9 (1996): 3673–81. http://dx.doi.org/10.1128/iai.64.9.3673-3681.1996.

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Ge, Zhongming, Yang Feng, Nancy S. Taylor, Masahiro Ohtani, Martin F. Polz, David B. Schauer, and James G. Fox. "Colonization Dynamics of Altered Schaedler Flora Is Influenced by Gender, Aging, and Helicobacter hepaticus Infection in the Intestines of Swiss Webster Mice." Applied and Environmental Microbiology 72, no. 7 (July 2006): 5100–5103. http://dx.doi.org/10.1128/aem.01934-05.

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ABSTRACT The distribution and colonization levels of the altered Schaedler flora (ASF) in their natural hosts are poorly understood. Intestinal colonization levels of the eight ASF strains in outbred Swiss Webster mice with or without Helicobacter hepaticus infection were characterized by real-time quantitative PCR. All ASF strains were detected in the cecum and colon, but some strains displayed significant variation in colonization levels with host age, gender, and H. hepaticus infection status.

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32

Belzer, Clara, Bart A. M. van Schendel, Ernst J. Kuipers, Johannes G. Kusters, and Arnoud H. M. van Vliet. "Iron-Responsive Repression of Urease Expression in Helicobacter hepaticus Is Mediated by the Transcriptional Regulator Fur." Infection and Immunity 75, no. 2 (November 13, 2006): 745–52. http://dx.doi.org/10.1128/iai.01163-06.

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ABSTRACT Persistent colonization of mucosal surfaces by bacteria in the mammalian host requires concerted expression of colonization factors, depending on the environmental conditions. Helicobacter hepaticus is a urease-positive pathogen that colonizes the intestinal and hepatobiliary tracts of rodents. Here it is reported that urease expression of H. hepaticus is iron repressed by the transcriptional regulator Fur. Iron restriction of growth medium resulted in a doubling of urease activity in wild-type H. hepaticus strain ATCC 51449 and was accompanied by increased levels of urease subunit pr

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33

Kullberg, Marika C., Dragana Jankovic, Peter L. Gorelick, Patricia Caspar, John J. Letterio, Allen W. Cheever, and Alan Sher. "Bacteria-triggered CD4+ T Regulatory Cells Suppress Helicobacter hepaticus–induced Colitis." Journal of Experimental Medicine 196, no. 4 (August 19, 2002): 505–15. http://dx.doi.org/10.1084/jem.20020556.

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We have previously demonstrated that interleukin (IL)-10–deficient (IL-10 knockout [KO]) but not wild-type (WT) mice develop colitis after infection with Helicobacter hepaticus. Here, we show that infected recombination activating gene (RAG) KO mice develop intestinal inflammation after reconstitution with CD4+ T cells from IL-10 KO animals and that the cotransfer of CD4+ T cells from H. hepaticus–infected but not uninfected WT mice prevents this colitis. The disease-protective WT CD4+ cells are contained within the CD45RBlow fraction and unexpectedly were found in both the CD25+ and the CD25−

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34

Feng, Sunlian, Karin Ku, Emir Hodzic, Edward Lorenzana, Kim Freet, and Stephen W. Barthold. "Differential Detection of Five Mouse-Infecting Helicobacter Species by Multiplex PCR." Clinical Diagnostic Laboratory Immunology 12, no. 4 (April 2005): 531–36. http://dx.doi.org/10.1128/cdli.12.4.531-536.2005.

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ABSTRACT Several species of helicobacter have been isolated from laboratory mice, including H. bilis, H. hepaticus, H. muridarum, H. rodentium, and H. typhlonius, which appear to be the most common. The most widely used published method for molecular detection of these agents is PCR amplification of a conserved region of 16S rRNA, but differential speciation requires restriction enzyme digestion of the amplicons. This study was undertaken to determine PCR conditions that would simultaneously and specifically identify each of the five common species without restriction enzyme analyses. First, w

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Yang, J., S. Ji, Y. Zhang, and J. Wang. "Helicobacter hepaticus infection in primary hepatocellular carcinoma tissue." Singapore Medical Journal 54, no. 8 (August 2013): 451–57. http://dx.doi.org/10.11622/smedj.2013153.

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36

Jiang, Qi, Yan-Qiang Huang, and Zan-Song Huang. "Relationship between Helicobacter hepaticus infection and hepatocellular carcinoma." World Chinese Journal of Digestology 22, no. 14 (2014): 1959. http://dx.doi.org/10.11569/wcjd.v22.i14.1959.

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37

Nilsson, Hans-Olof, Jalal Taneera, Maria Castedal, Elisabeth Glatz, Rolf Olsson, and Torkel Wadström. "Identification of Helicobacter pylori and OtherHelicobacter Species by PCR, Hybridization, and Partial DNA Sequencing in Human Liver Samples from Patients with Primary Sclerosing Cholangitis or Primary Biliary Cirrhosis." Journal of Clinical Microbiology 38, no. 3 (2000): 1072–76. http://dx.doi.org/10.1128/jcm.38.3.1072-1076.2000.

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Helicobacter pylori was identified in human liver tissue by PCR, hybridization, and partial DNA sequencing. Liver biopsies were obtained from patients with primary sclerosing cholangitis (n = 12), primary biliary cirrhosis (n = 12), and noncholestatic liver cirrhosis (n = 13) and (as controls) normal livers (n = 10). PCR analyses were carried out using primers for the Helicobacter genus, Helicobacter pylori(the gene encoding a species-specific 26-kDa protein and the 16S rRNA),Helicobacter bilis, Helicobacter pullorum, andHelicobacter hepaticus. Samples from patients with primary biliary cirrho

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Rogers, Arlin B., and James G. Fox. "Inflammation and Cancer I. Rodent models of infectious gastrointestinal and liver cancer." American Journal of Physiology-Gastrointestinal and Liver Physiology 286, no. 3 (March 2004): G361—G366. http://dx.doi.org/10.1152/ajpgi.00499.2003.

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Chronic gastrointestinal and liver infections account for a significant percentage of human cancer deaths. Rodent models help elucidate how infection can lead to malignancy. Helicobacter pylori, the leading cause of human gastric tumors, produces similar disease in Mongolian gerbils. H. pylori, H. felis, and H. hepaticus induce stomach, lower bowel, or liver tumors in susceptible wild-type and genetically engineered mice. Immune dysregulated mice recapitulate features of inflammatory bowel disease including colon carcinoma. Hepatitis B and C virus transgenic mice provide insights into viral he

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Taylor, N. S., J. G. Fox, and L. Yan. "In-vitro hepatotoxic factor in Helicobacter hepaticus, H. pylori and other Helicobacter species." Journal of Medical Microbiology 42, no. 1 (January 1, 1995): 48–52. http://dx.doi.org/10.1099/00222615-42-1-48.

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40

Patterson, M. M., M. D. Schrenzel, Y. Feng, S. Xu, F. E. Dewhirst, B. J. Paster, S. A. Thibodeau, J. Versalovic, and J. G. Fox. "Helicobacter aurati sp. nov., a Urease-Positive Helicobacter Species Cultured from Gastrointestinal Tissues of Syrian Hamsters." Journal of Clinical Microbiology 38, no. 10 (2000): 3722–28. http://dx.doi.org/10.1128/jcm.38.10.3722-3728.2000.

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A novel helicobacter with the proposed name Helicobacter aurati (type strain MIT 97-5075c) has been isolated from the inflamed stomachs and ceca of adult Syrian hamsters. The new species is fusiform with multiple bipolar sheathed flagella and periplasmic fibers; it contains urease and gamma-glutamyl transpeptidase. By 16S rRNA sequencing and repetitive element PCR-based DNA fingerprinting, it was found that H. aurati represents a distinct taxon and clusters with Helicobacter muridarum, Helicobacter hepaticus, and Helicobacter sp. MIT 94-022. H. aurati was recovered from hamsters housed in vari

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Mehta, Nalini S., Stephane Benoit, Jagannatha V. Mysore, Renato S. Sousa, and Robert J. Maier. "Helicobacter hepaticus Hydrogenase Mutants Are Deficient in Hydrogen-Supported Amino Acid Uptake and in Causing Liver Lesions in A/J Mice." Infection and Immunity 73, no. 9 (September 2005): 5311–18. http://dx.doi.org/10.1128/iai.73.9.5311-5318.2005.

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ABSTRACT Helicobacter hepaticus, a causative agent of chronic hepatitis and hepatocellular carcinoma in mice, expresses a nickel-containing hydrogen-oxidizing hydrogenase enzyme. Growth of a hyaB gene-targeted mutant was unaffected by the presence of hydrogen, unlike the wild-type strain, which showed an enhanced growth rate when supplied with H2. Hydrogenase activities in H. hepaticus were constitutive and not dependent on the inclusion of H2 during growth. Addition of nickel during growth significantly stimulated both urease (for wild-type and hyaB) and hydrogenase (for wild-type) activities

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Shen, Zeli, Yan Feng, and James G. Fox. "Cloning and sequencing of two Helicobacter hepaticus flagellin genes." Gastroenterology 118, no. 4 (April 2000): A326. http://dx.doi.org/10.1016/s0016-5085(00)83398-3.

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Foltz, C. J., J. G. Fox, L. Yan, and B. Shames. "Evaluation of antibiotic therapies for eradication of Helicobacter hepaticus." Antimicrobial Agents and Chemotherapy 39, no. 6 (June 1, 1995): 1292–94. http://dx.doi.org/10.1128/aac.39.6.1292.

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Morrison, P. J., D. Bending, L. A. Fouser, J. F. Wright, B. Stockinger, A. Cooke, and M. C. Kullberg. "Th17-cell plasticity in Helicobacter hepaticus–induced intestinal inflammation." Mucosal Immunology 6, no. 6 (March 6, 2013): 1143–56. http://dx.doi.org/10.1038/mi.2013.11.

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45

Nilsson, I. "Serum antibodies to Helicobacter hepaticus and Helicobacter pylori in patients with chronic liver disease." Gut 46, no. 3 (March 1, 2000): 410–14. http://dx.doi.org/10.1136/gut.46.3.410.

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lfeadike, W. C., M. A. Nicholson, K. A. Birkness, F. D. Quinn, E. H. White, G. W. Newman, J. H. Bartlett, D. Adams, and B. D. Gold. "17 COMPARISON OF HELICOBACTER PYLORI AND HELICOBACTER HEPATICUS INTERACTIONS WITH EUKARYOTIC CELLS IN VITRO." Journal of Pediatric Gastroenterology &amp Nutrition 23, no. 3 (October 1996): 346. http://dx.doi.org/10.1097/00005176-199610000-00047.

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Rogers, Arlin B., Samuel R. Boutin, Mark T. Whary, Nataliya Sundina, Zhongming Ge, Kathleen Cormier, and James G. Fox. "Progression of Chronic Hepatitis and Preneoplasia in Helicobacter hepaticus-Infected A/JCr Mice." Toxicologic Pathology 32, no. 6 (October 2004): 668–77. http://dx.doi.org/10.1080/01926230490524247.

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Fox, J. G., X. Li, L. Yan, R. J. Cahill, R. Hurley, R. Lewis, and J. C. Murphy. "Chronic proliferative hepatitis in A/JCr mice associated with persistent Helicobacter hepaticus infection: a model of helicobacter-induced carcinogenesis." Infection and immunity 64, no. 5 (1996): 1548–58. http://dx.doi.org/10.1128/iai.64.5.1548-1558.1996.

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SUERBAUM, S., C. JOSENHANS, M. FROSCH, M. BELL, K. BRAIG, P. BRANDT, B. CHEVREUX, G. DIETRICH, B. DRESCHER, and M. DROEGE. "Determining the whole genome sequence of Helicobacter hepaticus ATCC 51449." Gastroenterology 120, no. 5 (April 2001): A655. http://dx.doi.org/10.1016/s0016-5085(01)83258-3.

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Ge, Zhongming, Vincent B. Young, Chih Ching Chien, Nancy S. Taylor, David B. Schauer, and James G. Fox. "Functional characterization of the Helicobacter hepaticus cytolethal distending toxin operon." Gastroenterology 118, no. 4 (April 2000): A323. http://dx.doi.org/10.1016/s0016-5085(00)83384-3.

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