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Journal articles on the topic 'Helicobacter bilis'

Author: Grafiati

Published: 4 June 2021

Last updated: 2 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 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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2

Lemke, Laura B., Zhongming Ge, Mark T. Whary, Yan Feng, Arlin B. Rogers, Sureshkumar Muthupalani, and James G. Fox. "Concurrent Helicobacter bilis Infection in C57BL/6 Mice Attenuates Proinflammatory H. pylori-Induced Gastric Pathology." Infection and Immunity 77, no. 5 (February 17, 2009): 2147–58. http://dx.doi.org/10.1128/iai.01395-08.

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ABSTRACT Because coinfections can alter helicobacter gastritis, we investigated whether enterohepatic Helicobacter bilis modulates Helicobacter pylori gastritis in C57BL/6 mice. Thirty mice per group were sham dosed, H. bilis or H. pylori infected, or H. bilis infected followed in 2 weeks by H. pylori and then evaluated at 6 and 11 months postinfection (mpi) for gastritis and premalignant lesions. Compared to H. pylori-infected mice, H. bilis/H. pylori-infected mice at 6 and 11 mpi had less severe gastritis, atrophy, mucous metaplasia and hyperplasia (P < 0.01) and, additionally, at 11 mpi, less severe intestinal metaplasia and dysplasia (P < 0.05). H. bilis/H. pylori-infected mice at 11 mpi exhibited less Ki67 labeling of proliferating epithelial cells, reduced numbers of FoxP3+ T-regulatory (TREG) cells, and lower FoxP3+ mRNA levels than did H. pylori-infected mice (P < 0.05). Proinflammatory interleukin-1β (IL-1β), gamma interferon, and tumor necrosis factor alpha mRNA levels were attenuated in H. bilis/H. pylori-infected mice at 6 and 11 mpi (P < 0.01), although anti-inflammatory IL-10, IL-13, and transforming growth factor β1 mRNA levels were not consistently impacted by H. bilis coinfection. Decreased pathology in H. bilis/H. pylori-infected mice correlated with higher gastric H. pylori colonization at 6 mpi (P < 0.001) and lower Th1-associated immunoglobulin G2c responses to H. pylori at 6 and 10 mpi (P < 0.05). We hypothesized that reduced pathology in H. bilis/H. pylori-infected mice was due to H. bilis-primed TREG cells in the lower bowel that migrated to the gastric compartment and inhibited Th1 responses to subsequent H. pylori infection. Thus, H. pylori-induced gastric lesions may vary in mouse models of unknown enteric helicobacter infection status and, importantly, variable sequelae to human H. pylori infection, particularly in developing countries, may occur where coinfection with lower bowel helicobacters and H. pylori may be common.

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3

Han, S. R., C. Schindel, R. Genitsariotis, E. Märker-Hermann, S. Bhakdi, and M. J. Maeurer. "Identification of a Unique HelicobacterSpecies by 16S rRNA Gene Analysis in an Abdominal Abscess from a Patient with X-Linked Hypogammaglobulinemia." Journal of Clinical Microbiology 38, no. 7 (2000): 2740–42. http://dx.doi.org/10.1128/jcm.38.7.2740-2742.2000.

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A unique Helicobacter species, MZ640285, was isolated from a patient with X-linked hypogammaglobulinemia suffering from recurrent abdominal abscesses and was identified by 16S rRNA gene sequence analysis. In the phylogenetic tree, the isolate fell into a cluster which included Flexispira rappini,Helicobacter bilis, and Helicobacter sp. strain Mainz. Helicobacters are being increasingly recognized as pathogens in immunocompromised hosts. These fastidious bacteria are not easily cultured in the routine diagnostic laboratory, and this is the first report of their identification by 16S rRNA gene sequencing performed directly from a clinical specimen.

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4

Hänninen, M. L., R. I. Kärenlampi, J. M. K. Koort, T. Mikkonen, and K. J. Björkroth. "Extension of the species Helicobacter bilis to include the reference strains of Helicobacter sp. flexispira taxa 2, 3 and 8 and Finnish canine and feline flexispira strains." International Journal of Systematic and Evolutionary Microbiology 55, no. 2 (March 1, 2005): 891–98. http://dx.doi.org/10.1099/ijs.0.63245-0.

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The evolution and taxonomy of enterohepatic Helicobacter species with flexispira morphology were studied by a polyphasic approach including phenotypic characterization, analysis of 16S rRNA and ureB gene sequences and dot-blot DNA–DNA hybridization of whole genomic DNA. In addition, available phylogenetic data on the HSP60 gene were used in the analysis. The study included 14 Finnish canine and feline flexispira strains, the reference strains of Helicobacter sp. flexispira taxa 2, 3 and 8 and Helicobacter bilis ATCC 51630T. Phenotypically, all canine and feline strains were similar to H. bilis. Analysis of 16S rRNA gene sequences of these strains revealed a similarity of 97–99·5 %. Similarity of ureB nucleotide and amino acid sequences within the studied flexispira group was 97–100 % and 99–100 %, respectively, revealing close relatedness. ureB sequences of Helicobacter hepaticus had only 64–66 % similarity to the flexispira group. The similarity to Helicobacter trogontum was 81·5–82·1 %. High levels of DNA–DNA hybridization between the strains were found in dot-blot tests. Polyphasic analysis of the phenotypic and genotypic characteristics of the Finnish flexispira strains and the reference strains of taxa 2, 3 and 8 showed that they differed from other Helicobacter species and are members of the previously described species H. bilis. In addition, canine strain F56 differed in all phylogenetic analyses from the H. bilis group and probably represents a novel Helicobacter species.

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5

Jacobsen, K., E. Mahabir, M. Brielmeier, P. Wilhelm, K. E. Seidel, and J. Schmidt. "Monitoring a mouse colony for Helicobacter bilis using a Helicobacter-genus-specific nested PCR." Laboratory Animals 39, no. 4 (October 1, 2005): 400–412. http://dx.doi.org/10.1258/002367705774286402.

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Although Helicobacter infections of laboratory mice are usually subclinical, they may interfere with in vivo experiments and thus may lead to misinterpretation of data. As such, it is important to provide a means to unequivocally identify infections with murine Helicobacter spp. In the present study, a nested polymerase chain reaction (PCR) was established and shown to be 10 to 100 times more sensitive than the single-step PCR commonly used for routine diagnosis of Helicobacter spp. Experimental infection of Helicobacter-free mice demonstrated that faeces, caecum, colon and rectum but not liver are equally suitable for the detection of H. bilis. However, use of faecal pellets is advantageous since detection of H. bilis is possible one week after infection and analysis of faeces instead of tissues avoids euthanasia of animals. Furthermore, it generates representative data for all animals housed in the same cage and analysis can be repeatedly performed. Use of samples from breeding pairs but not offspring provides representative information about the Helicobacter status of a mouse colony. Both C3H/HeJ and C57BL/6 mice appear to be susceptible to H. bilis and persistent infection was observed during the 20-week experimental period. Analysis of pooled faecal pellets by nested PCR seems to be the most sensitive approach for H. bilis monitoring of the given breeding colony.

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6

Pisani, Paola, Mark T. Whary, Ingrid Nilsson, Supannee Sriamporn, Torkel Wadström, James G. Fox, Åsa Ljungh, and David Forman. "Cross-Reactivity between Immune Responses to Helicobacter bilis and Helicobacter pylori in a Population in Thailand at High Risk of Developing Cholangiocarcinoma." Clinical and Vaccine Immunology 15, no. 9 (July 2, 2008): 1363–68. http://dx.doi.org/10.1128/cvi.00132-08.

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ABSTRACT Helicobacter bilis DNA has been detected in human tissue and is a candidate for etiologic investigations on the causes of hepatic and biliary tract diseases, but reliable serologic tests need to be developed in order to pursue such investigations. The scope of this study was to assess the specificity of two assays for H. bilis immune response allowing for H. pylori, and their cross-reactivity in a population in Thailand at high risk for cholangiocarcinoma. Plasma samples from 92 Thai volunteers were independently tested in two laboratories (Massachusetts Institute of Technology [MIT] and Lund). MIT performed three analyses of H. pylori and H. bilis based either on (i) outer membrane protein (OMP) with no preabsorption or on antigens derived from whole-cell sonicate before (ii) or after (iii) preabsorption with H. pylori sonicate protein. Lund used cell surface proteins from H. pylori and H. bilis as antigens. Testing for H. bilis was preabsorbed with a whole-cell lysate of H. pylori. More than 80% of the samples were positive for H. pylori in both laboratories. As tested by MIT, 58.7% (95% confidence interval, 47.9 to 68.9%) were positive for H. bilis by OMP and 44.5% (34.1 to 55.3%) were positive for H. bilis sonicate protein, but only 15.2% (8.6 to 24.2%) remained positive after preabsorption with H. pylori sonicate protein. Lund found 34.5% of the samples positive for H. bilis (22.0 to 41.0%), which was statistically compatible with all three MIT results. Serologic responses to OMPs of the two bacteria coincided in 66 and 45% of the samples in the MIT and Lund assays, respectively. We found high cross-reactivity between the immune responses to H. pylori and H. bilis antigens. More-specific H. bilis antigens need to be isolated to develop serologic tests suitable for epidemiological studies.

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7

Rossi, Mirko, Renato Giulio Zanoni, and Marja-Liisa Hänninen. "Delineation of two Helicobacter bilis genomospecies: implications for systematics and evolution." International Journal of Systematic and Evolutionary Microbiology 60, no. 10 (October 1, 2010): 2392–97. http://dx.doi.org/10.1099/ijs.0.016287-0.

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The evolution and taxonomy of Helicobacter bilis strains isolated in Italy and Finland were studied by phylogenetic analysis of different genes, comparative analysis of small rRNA gene intervening sequence (IVS), amplified fragment length polymorphism analysis and DNA–DNA hybridization. The results of this study divided the H. bilis strains into two distinct and divergent genomic groups. In the absence of a specific phenotype or pathotype to distinguish these groups, however, they may be referred to as two genomospecies: H. bilis sensu stricto and Helicobacter sp. FL56. The phylogenetic network of gyrB and ureB gene sequences, as well as the comparative analysis of small rRNA gene IVS, suggests independent evolution of the two genomospecies. In particular, Helicobacter sp. FL56 seems to be the result of adaptation of an ancestral H. bilis strain in a new host. The phenomenon of adaptation to different hosts, or different intestinal niches in the same host, associated with high mutation and recombination rates could explain the evolution and the complex taxonomy of the genus Helicobacter. A comprehensive phylogenomics study of this genus would be useful to properly investigate this hypothesis.

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8

Feng, Sunlian, Lon V. Kendall, Emir Hodzic, Scott Wong, Edward Lorenzana, Kimberly Freet, Karin S. Ku, Paul A. Luciw, Stephen W. Barthold, and Imran H. Khan. "Recombinant Helicobacter bilis Protein P167 for Mouse Serodiagnosis in a Multiplex Microbead Assay." Clinical Diagnostic Laboratory Immunology 11, no. 6 (November 2004): 1094–99. http://dx.doi.org/10.1128/cdli.11.6.1094-1099.2004.

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ABSTRACT Infection of mice with Helicobacter bilis is widespread in research and commercial mouse colonies. Therefore, sensitive, specific, and high-throughput assays are needed for rapid and accurate testing of mice in large numbers. This report describes a novel multiplex assay, based on fluorescent microbeads, for serodetection of H. bilis infection. The assay requires only a few microliters of serum to perform and is amenable to a high-throughput format. Individual microbead sets were conjugated to purified, H. bilis-specific, recombinant proteins P167C and P167D and bacterial membrane extracts from H. bilis and Helicobacter hepaticus. For detecting H. bilis infection in the microbead multiplex assay, P167C and P167D provided significantly higher sensitivities (94 and 100%, respectively) and specificities (100 and 95%, respectively) than membrane extract (78% sensitivity and 65% specificity). Microbead multiplex assay results were validated by enzyme-linked immunosorbent assay. Purified recombinant proteins showed low batch-to-batch variation; this feature allows for ease of quality control, assay robustness, and affordability. Thus, recombinant antigens are highly suitable in the multiplex microbead assay format for serodetection of H. bilis infection.

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9

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 dilution of 1:800 in an enzyme-linked immunosorbent assay. Sera from mice experimentally infected with H. hepaticus did not react with P167C and P167D. Sera from mice naturally infected with H. bilis but not sera from mice naturally infected with H. hepaticus reacted with P167C and P167D. Hyperimmune sera against P167C peptide reacted with recombinant P167C and with a 120-kDa band in H. bilis lysates but did not react with a protein of the same size on immunoblots prepared from H. hepaticus, H. muridarum, or unrelated Borrelia burgdorferi and Campylobacter jejuni whole-cell lysates. Nevertheless, the P167A, P167B, P167C, and P167D primers, but not the P167E primers, amplified DNA from H. hepaticus, and all five primer sets amplified DNA from H. muridarum. These results suggest that P167 is an immunodominant, H. bilis-specific antigen that may have potential for use in serodiagnosis.

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10

Ge, Zhongming, Peter Doig, and James G. Fox. "Characterization of Proteins in the Outer Membrane Preparation of a Murine Pathogen, Helicobacter bilis." Infection and Immunity 69, no. 5 (May 1, 2001): 3502–6. http://dx.doi.org/10.1128/iai.69.5.3502-3506.2001.

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ABSTRACT Helicobacter bilis is a bacterial pathogen associated with multifocal hepatitis and inflammatory bowel disease in certain strains of mice. This bacterium colonizes the liver, bile, and lower intestine in mice and has also been isolated from a wide spectrum of laboratory animals. In this study, proteins present in the outer membrane preparation (OMP) of four H. bilis strains isolated from a mouse, a dog, a rat, and a gerbil were characterized and compared with that of Helicobacter pylori, a human gastric pathogen. All four H. bilis strains had similar OMP protein profiles that were distinct from those of H. pylori. Immunoblotting demonstrated that OMP proteins fromH. bilis and H. pylori have little cross-reactivity, except for their flagellins. Nine major immunogenic polypeptides were present in the H. bilis OMPs. By using two-dimensional sodium dodecyl sulfate-polyacrylamide gel electrophoresis, five heat-modifiable proteins with molecular masses of 82, 66, 52, 47 and 37 kDa were identified. The N-terminal sequences of the 46- and 47-kDa OMP proteins had no homology with protein sequences available in public databases. These results indicate that H. bilis has a conserved, unique OMP protein profile that is distinct from those of H. pylori.

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11

Haines, D. C., P. L. Gorelick, J. K. Battles, K. M. Pike, R. J. Anderson, J. G. Fox, N. S. Taylor, et al. "Inflammatory Large Bowel Disease in Immunodeficient Rats Naturally and Experimentally Infected with Helicobacter bilis." Veterinary Pathology 35, no. 3 (May 1998): 202–8. http://dx.doi.org/10.1177/030098589803500305.

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Proliferative and ulcerative typhlitis, colitis, and proctitis were found incidentally in a breeding colony of male athymic nude (Cr:NIH-rnu) rats. Within the crypts of the large intestine, modified Steiner's silver stain revealed spiral organisms that were identified by culture, polymerase chain reaction, and sequencing to be Helicobacter bilis. The large bowel disease was reproduced in H. bilis-free male athymic nude rats that were injected intraperitoneally with a culture of H. bilis from the affected colony. The organism was isolated from the feces and cecum of the experimentally infected rats. H. bilis should be considered a potential pathogen in immunocompromised rats. The infection in immunocompromised rats may serve as an animal model for inflammatory large bowel disease.

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12

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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13

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 histopathological IBD phenotype. IL-10−/−mice developed severe diffuse IBD with either H. bilis or H. hepaticus, whereas Rag1−/−, TCR-α−/−, TCR-β−/−, and wild-type mice showed different susceptibilities to Helicobacter spp infection. Proinflammatory cytokine mRNA expression was increased in the colons of Helicobacter-infected IL-10−/−and TCR-α−/−mice with IBD. These results confirm and extend the role of Helicobacter as a useful tool for investigating microbial-induced IBD and show the importance, but not strict dependence, of T cells in the development of bacterial-induced IBD.

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14

Murata, H., S. Tsuji, M. Tsujii, H. Y. Fu, H. Tanimura, M. Tsujimoto, N. Matsuura, S. Kawano, and M. Hori. "Helicobacter bilis infection in biliary tract cancer." Alimentary Pharmacology & Therapeutics 20 (July 2004): 90–94. http://dx.doi.org/10.1111/j.1365-2036.2004.01972.x.

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15

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, we designed novel and specific PCR primers for H. bilis, H. hepaticus, H. muridarum, H. rodentium, and H. typhlonius, using sequences from the heterologous regions of 16S rRNA. Because of comigration of amplified products, we next identified P17, an H. bilis-specific protein; P25, an H. hepaticus-specific protein; and P30, an H. muridarum-specific protein by screening genomic DNA expression libraries of each species. Primers were designed from these three genes, plus newly designed, species-specific 16S rRNA primers for H. rodentium and H. typhlonius that could be utilized for a five-plex PCR. The sizes of the amplicons from H. bilis, H. hepaticus, H. muridarum, H. rodentium, and H. typhlonius were 435, 705, 807, 191, and 122 bp, respectively, allowing simultaneous detection and effective discrimination among species.

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Muthupalani, Sureshkumar, Zhongming Ge, Yan Feng, Barry Rickman, Melissa Mobley, Amanda McCabe, Nico Van Rooijen, and James G. Fox. "Systemic Macrophage Depletion Inhibits Helicobacter bilis-Induced Proinflammatory Cytokine-Mediated Typhlocolitis and Impairs Bacterial Colonization Dynamics in a BALB/cRag2−/−Mouse Model of Inflammatory Bowel Disease." Infection and Immunity 80, no. 12 (October 1, 2012): 4388–97. http://dx.doi.org/10.1128/iai.00530-12.

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ABSTRACTHelicobacter bilis, an enterohepatic helicobacter, is associated with chronic hepatitis in aged immunocompetent inbred mice and inflammatory bowel disease (IBD) in immunodeficient mice. To evaluate the role of macrophages inH. bilis-induced IBD,Rag2−/−BALB/c or wild-type (WT) BALB/c mice were either sham dosed or infected withH. bilisMissouri strain under specific-pathogen-free conditions, followed by an intravenous injection of a 0.2-ml suspension of liposomes coated with either phosphate-buffered saline (control) or clodronate (a macrophage depleting drug) at 15 weeks postinfection (wpi). At 16 wpi, the ceca ofH. bilis-infectedRag2−/−mice treated with control liposomes had significantly higher histopathological lesional scores (for cumulative typhlitis index, inflammation, edema, epithelial defects, and hyperplasia) and higher counts of F4/80+macrophages and MPO+neutrophils compared toH. bilis-infectedRag2−/−mice treated with clodronate liposomes. In addition, cecal quantitative PCR analyses revealed a significant suppression in the expression of macrophage-related cytokine genes, namely,Tnfa,Il-1β,Il-10,Cxcl1, andiNos, in the clodronate-treatedH. bilis-infectedRag2−/−mice compared to theH. bilis-infectedRag2−/−control mice. Finally, cecal quantitative PCR analyses also revealed a significant reduction in bacterial colonization in the clodronate-treatedRag2−/−mice. Taken together, our results suggest that macrophages are critical inflammatory cellular mediators for promotingH. bilis-induced typhlocolitis in mice.

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17

Henderson, A., A. Ramer-Tait, A. Dorn, J. Hostetter, A. Jergens, and M. Wannemuehler. "Helicobacter bilis colonization enhances susceptibility to DSS-induced colitis." Inflammatory Bowel Diseases 14 (December 2008): S8. http://dx.doi.org/10.1097/00054725-200812001-00024.

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18

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 cirrhosis and primary sclerosing cholangitis (11 and 9 samples, respectively) were positive by PCR with Helicobactergenus-specific primers. Of these 20 samples, 8 were positive with the 16S rRNA primer and 9 were positive with the 26-kDa protein primer ofH. pylori. These nine latter samples were also positive by Southern blot hybridization for the amplified 26-kDa fragment, and four of those were verified to be H. pylori by partial 16S rDNA sequencing. None of the samples reacted with primers for H. bilis, H. pullorum, or H. hepaticus. None of the normal livers had positive results in theHelicobacter genus PCR assay, and only one patient in the noncholestatic liver cirrhosis group, a young boy who at reexamination showed histological features suggesting primary sclerosing cholangitis, had a positive result in the same assay. Helicobacterpositivity was thus significantly more common in patients with cholestatic diseases (20 of 24) than in patients with noncholestatic diseases and normal controls (1 of 23) (P = <0.00001). Patients positive for Helicobacter genus had significantly higher values of alkaline phosphatases and prothrombin complex than Helicobacter-negative patients (P = 0.0001 and P = 0.0003, respectively). Among primary sclerosing cholangitis patients,Helicobacter genus PCR positivity was weakly associated with ulcerative colitis (P = 0.05). Significant differences related to blood group or HLA status were not found.

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19

Roosendaal, Robert, Jan H. Vos, Thijs Roumen, René van Vugt, Giovanni Cattoli, Aldert Bart, Henricus L. B. M. Klaasen, Ernst J. Kuipers, Christina M. J. E. Vandenbroucke-Grauls, and Johannes G. Kusters. "Slaughter Pigs Are Commonly Infected by Closely Related but Distinct Gastric Ulcerative Lesion-Inducing Gastrospirilla." Journal of Clinical Microbiology 38, no. 7 (2000): 2661–64. http://dx.doi.org/10.1128/jcm.38.7.2661-2664.2000.

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An association between (unculturable) gastrospirillum-like organisms (GLO) and ulcerative lesions in the pars oesophagea in stomachs of swine has been claimed. In dogs GLO detected by microscopy may represent several Helicobacter species or subspecies. Therefore we investigated which Helicobacter spp. are present in stomachs of swine and their possible association with ulcerative lesions of the pars oesophagea. The presence ofHelicobacter spp. in the antrum and pars oesophagea in 122 stomachs of slaughter swine was determined by microscopy (n = 122), by culture on selective and nonselective media (n = 112), and by a genus-specific 16S ribosomal DNA (rDNA) PCR (n = 80). GLO could not be cultured. Phylogenetic analysis of 43 16S rDNA fragments (out of 54 PCR-positive biopsy specimens) revealed the presence of Helicobacter heilmannii type 1 in 42 of them. This correlated with the presence of bacteria with GLO morphology. Helicobacter bilis 16S rDNA was amplified directly from one sample harboring bacteria with H. bilis morphology. The association betweenHelicobacter spp. and gastric lesions was investigated with a second group of 41 pigs with (n = 21 cases) or without (n = 20 controls) gastric lesions. Fifteen of the 21 cases were positive by PCR or microscopy, compared to 7 of 20 of the controls (P = 0.03). 16S rDNA sequence analysis of 7 of 14 PCR-positive cases revealed the presence of H. heilmannii type 1. Microscopy showed bacteria with GLO morphology. One sample (cases) was culture negative but PCR positive for Helicobacter pullorum-related 16S rDNA. In conclusion, our findings indicate that H. heilmannii type 1 is the predominant Helicobacter spp. in the stomachs of pigs and that its presence is associated with ulcerative lesions in the pars oesophagea.

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Whary, Mark T., Chuanwu Wang, Catherine F. Ruff, Mallory J. DiVincenzo, Caralyn Labriola, Lillian Ge, Yan Feng, et al. "Effects of Colonization of Gnotobiotic Swiss Webster Mice with Helicobacter bilis." Comparative Medicine 70, no. 3 (June 1, 2020): 216–32. http://dx.doi.org/10.30802/aalas-cm-19-000087.

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Helicobacter bilis (Hb) causes hepatitis in some strains of inbred mice. The current study confirmed that Hb directly causes portal hepatitis in outbred gnotobiotic Swiss Webster (SW) mice, as we previously reported for conventional SW mice. Hbmonoassociated SW mice also developed mild enterocolitis, expanded gut-associated lymphoid tissue (GALT), and tertiary lymphoid tissue in the lower bowel. At 1 and 10 mo after infection, Hb-induced GALT hyperplasia exhibited well-organized, ectopic germinal centers with increased mononuclear cell apoptosis, MHC class II antigen presentation, and pronounced endothelial venule formation, consistent with features of tertiary lymphoid tissue. In the lower bowel, Hb induced mainly B220+ cells as well as CD4+ IL17+, CD4+ IFNγ+, and CD4+ FoxP3+ regulatory T cells and significantly increased IL10 mRNA expression. This gnotobiotic model confirmed that Hb causes portal hepatitis in outbred SW mice but stimulated GALT with an antiinflammatory bias. Because Hb had both anti- and proinflammatory effects on GALT, it should be considered a 'pathosymbiont provocateur' and merits further evaluation in mouse models of human disease.

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Takayama, Satoru, Hiroki Takahashi, Yoichi Matsuo, Yuji Okada, and Hiromitsu Takeyama. "Effect of Helicobacter bilis Infection on Human Bile Duct Cancer Cells." Digestive Diseases and Sciences 55, no. 7 (September 3, 2009): 1905–10. http://dx.doi.org/10.1007/s10620-009-0946-6.

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Liu, Zhiping, Amanda E. Ramer-Tait, Abigail L. Henderson, Cumhur Yusuf Demirkale, Dan Nettleton, Chong Wang, Jesse M. Hostetter, Albert E. Jergens, and Michael J. Wannemuehler. "Helicobacter bilis Colonization Enhances Susceptibility to Typhlocolitis Following an Inflammatory Trigger." Digestive Diseases and Sciences 56, no. 10 (April 19, 2011): 2838–48. http://dx.doi.org/10.1007/s10620-011-1701-3.

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Wasimuddin, Dagmar Čížková, Josef Bryja, Jana Albrechtová, Heidi C. Hauffe, and Jaroslav Piálek. "High Prevalence and Species Diversity of Helicobacter spp. Detected in Wild House Mice." Applied and Environmental Microbiology 78, no. 22 (September 7, 2012): 8158–60. http://dx.doi.org/10.1128/aem.01989-12.

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ABSTRACTPCR diagnostics detected 100% prevalence ofHelicobacterin 425 wild house mice (Mus musculus) from across central Europe. Of seven species identified, the five most frequent wereHelicobacter rodentium(78%),H. typhlonius(53%),H. hepaticus(41%),H. bilis(30%), andH. muridarum(1%). Double infections were more common (42%) than single (30%) and triple (21%) infections. Wild house mice could be considered potential reservoirs ofHelicobacterstrains for both humans and other vertebrates.

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Shomer, N. H., C. A. Dangler, M. D. Schrenzel, and J. G. Fox. "Helicobacter bilis-induced inflammatory bowel disease in scid mice with defined flora." Infection and immunity 65, no. 11 (1997): 4858–64. http://dx.doi.org/10.1128/iai.65.11.4858-4864.1997.

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Kosaka, T., Y. Tajima, T. Kuroki, T. Mishima, T. Adachi, N. Tsuneoka, K. Fukuda, and T. Kanematsu. "Helicobacter bilis colonization of the biliary system in patients with pancreaticobiliary maljunction." British Journal of Surgery 97, no. 4 (February 12, 2010): 544–49. http://dx.doi.org/10.1002/bjs.6907.

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Atherly, Todd, Curtis Moser, Jesse Hostetter, Chong Wang, Alexandra Proctor, Gregory Phillips, Meghan Wymore Brand, Michael Wannemuehler, and Albert Jergens. "P-138 Helicobacter Bilis Infection Alters Mucosal Bacteria in Defined Microbiota Mice." Inflammatory Bowel Diseases 22 (March 2016): S52. http://dx.doi.org/10.1097/01.mib.0000480243.16265.e0.

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Turvey, Stuart E., Sara H. Leo, Annette Boos, Gregory D. Deans, Julie Prendiville, Richard I. Crawford, Christof Senger, et al. "Successful Approach to Treatment of Helicobacter bilis Infection in X-Linked Agammaglobulinemia." Journal of Clinical Immunology 32, no. 6 (July 28, 2012): 1404–8. http://dx.doi.org/10.1007/s10875-012-9750-8.

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Degand, Nicolas, Justine Dautremer, Benoît Pilmis, Agnès Ferroni, Fanny Lanternier, Julie Bruneau, Olivier Hermine, et al. "Helicobacter bilis-Associated Suppurative Cholangitis in a Patient with X-Linked Agammaglobulinemia." Journal of Clinical Immunology 37, no. 7 (August 31, 2017): 727–31. http://dx.doi.org/10.1007/s10875-017-0437-z.

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29

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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Fox, J. G., L. L. Yan, F. E. Dewhirst, B. J. Paster, B. Shames, J. C. Murphy, A. Hayward, J. C. Belcher, and E. N. Mendes. "Helicobacter bilis sp. nov., a novel Helicobacter species isolated from bile, livers, and intestines of aged, inbred mice." Journal of clinical microbiology 33, no. 2 (1995): 445–54. http://dx.doi.org/10.1128/jcm.33.2.445-454.1995.

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Atherly, Todd, Curtis Mosher, Chong Wang, Jesse Hostetter, Alexandra Proctor, Meghan W. Brand, Gregory J. Phillips, Michael Wannemuehler, and Albert E. Jergens. "Helicobacter bilis Infection Alters Mucosal Bacteria and Modulates Colitis Development in Defined Microbiota Mice." Inflammatory Bowel Diseases 22, no. 11 (November 2016): 2571–81. http://dx.doi.org/10.1097/mib.0000000000000944.

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32

Maggio-Price, Lillian, Helle Bielefeldt-Ohmann, Piper Treuting, Brian M. Iritani, Weiping Zeng, Andrea Nicks, Mark Tsang, Donna Shows, Phil Morrissey, and Joanne L. Viney. "Dual Infection with Helicobacter bilis and Helicobacter hepaticus in P-Glycoprotein-Deficient mdr1a−/− Mice Results in Colitis that Progresses to Dysplasia." American Journal of Pathology 166, no. 6 (June 2005): 1793–806. http://dx.doi.org/10.1016/s0002-9440(10)62489-3.

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Javed, Sundus, Raquel Mejías-Luque, Behnam Kalali, Christian Bolz, and Markus Gerhard. "Helicobacter bilis Gamma-Glutamyltranspeptidase Enhances Inflammatory Stress Response via Oxidative Stress in Colon Epithelial Cells." PLoS ONE 8, no. 8 (August 23, 2013): e73160. http://dx.doi.org/10.1371/journal.pone.0073160.

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34

Kostomitsopoulos, Nikolaos, Harry Donnelly, Ioanna Kostavasili, Euthimios Paronis, Paul Alexakos, and Panayotis Karayannacos. "Eradication of Helicobacter bilis and H. hepaticus from infected mice by using a medicated diet." Lab Animal 36, no. 5 (May 2007): 37–40. http://dx.doi.org/10.1038/laban0507-37.

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35

Jergens, Albert, Todd A. Atherly, Robert T. Doyle, Abigail Henderson, Kelley M. Clausen, Cherie Ziemer, and Michael J. Wannemuehler. "W1202 Helicobacter bilis Infection Alters the Spatial Distribution of Commensal Bacteria in Colitic C3h/Hen Mice." Gastroenterology 134, no. 4 (April 2008): A—654. http://dx.doi.org/10.1016/s0016-5085(08)63052-8.

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36

Thanaphongdecha, Prissadee, Shannon E. Karinshak, Wannaporn Ittiprasert, Victoria H. Mann, Yaovalux Chamgramol, Chawalit Pairojkul, James G. Fox, Sutas Suttiprapa, Banchob Sripa, and Paul J. Brindley. "Infection with Helicobacter pylori Induces Epithelial to Mesenchymal Transition in Human Cholangiocytes." Pathogens 9, no. 11 (November 21, 2020): 971. http://dx.doi.org/10.3390/pathogens9110971.

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Recent reports suggest that the East Asian liver fluke infection, caused by Opisthorchis viverrini, which is implicated in opisthorchiasis-associated cholangiocarcinoma, serves as a reservoir of Helicobacter pylori. The opisthorchiasis-affected cholangiocytes that line the intrahepatic biliary tract are considered to be the cell of origin of this malignancy. Here, we investigated interactions in vitro among human cholangiocytes, Helicobacter pylori strain NCTC 11637, and the congeneric bacillus, Helicobacter bilis. Exposure to increasing numbers of H. pylori at 0, 1, 10, 100 bacilli per cholangiocyte of the H69 cell line induced phenotypic changes including the profusion of thread-like filopodia and a loss of cell-cell contact, in a dose-dependent fashion. In parallel, following exposure to H. pylori, changes were evident in levels of mRNA expression of epithelial to mesenchymal transition (EMT)-encoding factors including snail, slug, vimentin, matrix metalloprotease, zinc finger E-box-binding homeobox, and the cancer stem cell marker CD44. Analysis to quantify cellular proliferation, migration, and invasion in real-time by both H69 cholangiocytes and CC-LP-1 line of cholangiocarcinoma cells using the xCELLigence approach and Matrigel matrix revealed that exposure to ≥10 H. pylori bacilli per cell stimulated migration and invasion by the cholangiocytes. In addition, 10 bacilli of H. pylori stimulated contact-independent colony establishment in soft agar. These findings support the hypothesis that infection by H.pylori contributes to the malignant transformation of the biliary epithelium.

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Foley, Janet E., Stanley L. Marks, Linda Munson, Ann Melli, Floyd E. Dewhirst, Shilu Yu, Zeli Shen, and James G. Fox. "Isolation of Helicobacter canis from a Colony of Bengal Cats with Endemic Diarrhea." Journal of Clinical Microbiology 37, no. 10 (1999): 3271–75. http://dx.doi.org/10.1128/jcm.37.10.3271-3275.1999.

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On the basis of biochemical, phenotypic, and 16S rRNA analyses,Helicobacter canis was isolated from Bengal cats with and without chronic diarrhea. Because the cats were coinfected with other potential pathogens, including Campylobacter helveticus, and because H. canis was isolated from nondiarrheic cats, the causal role of H. canis in producing the diarrhea could not be proven. Histologically, the colons of the four affected cats were characterized by mild to moderate neutrophilic, plasmacytic, and histocytic infiltrates in the lamina propria. Rare crypt abscesses were also noted for three cats but were a more prominent feature of the colonic lesions noted for the fourth cat. This is the first observation of H. canis in cats and raises the possibility thatH. canis, like H. hepaticus and H. bilis in mice, can cause inflammation of the colon, particularly in hosts with immune dysregulation. Further studies are needed to determine the importance of H. canis as a primary enteric pathogen in cats and the role of cats in the possible zoonotic spread of H. canis to humans.

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Ramer-Tait, A., A. Henderson, J. Hostetter, A. Jergens, and M. Wannemuehler. "Selective colonization with Helicobacter bilis or Escherichia coli induces differential host immune responses following an inflammatory trigger." Inflammatory Bowel Diseases 17 (January 2011): S1. http://dx.doi.org/10.1002/ibd.21581.

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Ramer-Tait, Amanda E., Abigail Henderson, Jesse Hostetter, Albert Jergens, and Michael J. Wannemuehler. "T1791 Selective Colonization With Helicobacter bilis or Escherichia coli Induces Differential Host Immune Responses Following a Colitic Insult." Gastroenterology 138, no. 5 (May 2010): S—579. http://dx.doi.org/10.1016/s0016-5085(10)62669-8.

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Jergens, A. E., J. H. Wilson-Welder, A. Dorn, A. Henderson, Z. Liu, R. B. Evans, J. Hostetter, and M. J. Wannemuehler. "Helicobacter bilis triggers persistent immune reactivity to antigens derived from the commensal bacteria in gnotobiotic C3H/HeN mice." Gut 56, no. 7 (July 1, 2007): 934–40. http://dx.doi.org/10.1136/gut.2006.099242.

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41

Fox, J. G. "Helicobacter bilis: bacterial provocateur orchestrates host immune responses to commensal flora in a model of inflammatory bowel disease." Gut 56, no. 7 (July 1, 2007): 898–900. http://dx.doi.org/10.1136/gut.2006.115428.

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42

Liu, Zhiping, Abigail L. Henderson, Dan Nettleton, Jennifer H. Wilson-Welder, Jesse M. Hostetter, Amanda Ramer-Tait, Albert E. Jergens, and Michael J. Wannemuehler. "Mucosal gene expression profiles following the colonization of immunocompetent defined-flora C3H mice with Helicobacter bilis: a prelude to typhlocolitis." Microbes and Infection 11, no. 3 (March 2009): 374–83. http://dx.doi.org/10.1016/j.micinf.2008.12.013.

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43

Maggio-Price, Lillian, Donna Shows, Kim Waggie, Andrew Burich, Weiping Zeng, Sabine Escobar, Phil Morrissey, and Joanne L. Viney. "Helicobacter bilis Infection Accelerates and H. hepaticus Infection Delays the Development of Colitis in Multiple Drug Resistance-Deficient (mdr1a−/−) Mice." American Journal of Pathology 160, no. 2 (February 2002): 739–51. http://dx.doi.org/10.1016/s0002-9440(10)64894-8.

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44

Jergens, Albert E., Andrea Dorn, Jenny Wilson, Krystal Dingbaum, Abigail Henderson, Zhiping Liu, Jesse Hostetter, Richard B. Evans, and Michael J. Wannemuehler. "Induction of differential immune reactivity to members of the flora of gnotobiotic mice following colonization with Helicobacter bilis or Brachyspira hyodysenteriae." Microbes and Infection 8, no. 6 (May 2006): 1602–10. http://dx.doi.org/10.1016/j.micinf.2006.01.019.

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45

Seamons, Audrey, Michael Haenisch, Stacey Meeker, Olesya Pershutkina, Thea Brabb, Piper M. Treuting, and Jisun Paik. "Protective Effects of ALDH1A Enzyme Inhibition on Helicobacter-Induced Colitis in Smad3−/− Mice are Associated with Altered α4ß7 Integrin Expression on Activated T Cells." Nutrients 12, no. 10 (September 24, 2020): 2927. http://dx.doi.org/10.3390/nu12102927.

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Many inflammatory bowel disease (IBD) patients require surgical intervention due to limited pharmacological treatment options. Antibodies targeting α4ß7, a gut-homing integrin, are one of the most promising IBD treatments. As retinoic acid (RA) regulates expression of gut-homing proteins including α4ß7 integrin, we tested if ALDH1A enzymes in the RA synthesis pathway could be targeted for IBD treatment using a potent inhibitor, WIN 18,446. Age- and sex-matched Smad3−/− mice were fed a diet with and without WIN 18,446 for 3 weeks before triggering inflammation with Helicobacter bilis infection. Colitis was evaluated by histopathology one week following the IBD trigger, and T cell subsets were evaluated before and after the IBD trigger. WIN 18,446 treatment significantly reduced IBD severity in Smad3−/− mice and reduced expression of α4ß7 integrin on multiple activated CD4+ T cell subsets. This change was associated with increased ratios of induced regulatory T cells to Th17 cells during the inflammatory response in the draining lymph nodes. These studies indicate that RA reduction via ALDH1A enzyme inhibition is a potential new target for IBD treatment. Further studies are needed to examine its effects on other types of immune cells, to evaluate the efficacy window for this target, and to determine its efficacy in other animal models of IBD.

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Fox, J. G., Z. Shen, S. Muthupalani, A. R. Rogers, S. M. Kirchain, and F. E. Dewhirst. "Chronic Hepatitis, Hepatic Dysplasia, Fibrosis, and Biliary Hyperplasia in Hamsters Naturally Infected with a Novel Helicobacter Classified in the H. bilis Cluster." Journal of Clinical Microbiology 47, no. 11 (September 16, 2009): 3673–81. http://dx.doi.org/10.1128/jcm.00879-09.

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Wang, Jin, Tianfang Wang, Yanfang Sun, Yuan Feng, William Kisseberth, Carolyn Henry, Irene Mok, et al. "Proliferative and Invasive Colorectal Tumors in Pet Dogs Provide Unique Insights into Human Colorectal Cancer." Cancers 10, no. 9 (September 14, 2018): 330. http://dx.doi.org/10.3390/cancers10090330.

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Spontaneous tumors in pet dogs represent a valuable but undercharacterized cancer model. To better use this resource, we performed an initial global comparison between proliferative and invasive colorectal tumors from 20 canine cases, and evaluated their molecular homology to human colorectal cancer (CRC). First, proliferative canine tumors harbor overactivated WNT/β-catenin pathways and recurrent CTNNB1 (β-catenin) mutations S45F/P, D32Y and G34E. Invasive canine tumors harbor prominent fibroblast proliferation and overactivated stroma. Both groups have recurrent TP53 mutations. We observed three invasion patterns in canine tumors: collective, crypt-like and epithelial–mesenchymal transition (EMT). We detected enriched Helicobacter bilis and Alistipes finegoldii in proliferative and crypt-like tumors, but depleted mucosa-microbes in the EMT tumor. Second, guided by our canine findings, we classified 79% of 478 human colon cancers from The Cancer Genome Atlas into four subtypes: primarily proliferative, or with collective, crypt-like or EMT invasion features. Their molecular characteristics match those of canine tumors. We showed that consensus molecular subtype 4 (mesenchymal) of human CRC should be further divided into EMT and crypt-like subtypes, which differ in TGF-β activation and mucosa-microbe content. Our canine tumors share the same pathogenic pathway as human CRCs. Dog-human integration identifies three CRC invasion patterns and improves CRC subtyping.

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Fu, X., and W. Peng. "Helicobacter bilis may play a role in the carcinogenesis of colitis associated colon cancer correlating to increased number of CD4+CD45RB+ T cells." Annals of Oncology 30 (November 2019): ix31. http://dx.doi.org/10.1093/annonc/mdz421.005.

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49

Danon, Stephen J., Minoo J. Moghaddam, and Vanessa Stebbings. "W1200 An Oral Prophylactic Vaccine Comprised of Helicobacter bilis Antigens Encapsulated in a Self Assembled Tris Cationic Lipid Prevents IBD-Like Disease in IL-10 Deficient Mice." Gastroenterology 134, no. 4 (April 2008): A—653. http://dx.doi.org/10.1016/s0016-5085(08)63050-4.

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Goto, Kazuo, Hideki Horiuchi, Haruka Shinohara, Katsumi Motegi, Koji Hashimoto, Sadato Hongo, Nobuhiro Gemma, Nobuhito Hayashimoto, Toshio Itoh, and Akira Takakura. "Specific and quantitative detection of PCR products from Clostridium piliforme, Helicobacter bilis, H. hepaticus, and mouse hepatitis virus infected mouse samples using a newly developed electrochemical DNA chip." Journal of Microbiological Methods 69, no. 1 (April 2007): 93–99. http://dx.doi.org/10.1016/j.mimet.2006.12.009.

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