Journal articles: 'Helicobacter hepaticus'

1

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

Full text

Abstract:

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.

APA, Harvard, Vancouver, ISO, and other styles

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.

Full text

Abstract:

Helicobacter hepaticus is a pathogen of rodents, which causes diverse enteric and hepatic inflammatory diseases and malignancies. The urease enzyme is an important colonization factor of gastric Helicobacter species like Helicobacter pylori, but little is known about the role and regulation of urease in enterohepatic Helicobacter species. Here it is reported that urease activity of H. hepaticus does not contribute to acid resistance, and that it is nickel-responsive at the post-translational level. H. hepaticus strain ATCC 51449 did not grow or survive at pH 3·0, and supplementation with urea or NiCl2 did not abrogate this acid sensitivity. Furthermore, urease enzyme activity of H. hepaticus was acid-independent, which contrasts with the acid-induced urease system of H. pylori. Nickel supplementation of Brucella medium resulted in a tenfold increase in urease activity in both H. hepaticus and H. pylori, but the maximum level of urease activity in H. hepaticus was still three- to fivefold lower when compared to H. pylori in the same conditions. The increase in urease activity of H. hepaticus was not associated with elevation of urease mRNA or protein levels. Inhibition of protein synthesis by chloramphenicol did not affect nickel-responsive induction of urease activity in H. hepaticus, and confirmed that nickel induction occurs at the post-translational level, probably by activation of preformed apo-enzyme. In conclusion, both the role of the urease enzyme and the regulation of urease activity differ between the enterohepatic pathogen H. hepaticus and the gastric pathogen H. pylori.

APA, Harvard, Vancouver, ISO, and other styles

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.

Full text

Abstract:

ABSTRACT Helicobacter hepaticus is a gram-negative, spiral-shaped microaerophilic bacterium associated with chronic intestinal infection leading to hepatitis and colonic and hepatic carcinomas in susceptible strains of mice. In the closely related human pathogen Helicobacter pylori, l-proline is a preferred respiratory substrate and is found at significantly high levels in the gastric juice of infected patients. A previous study of the proline catabolic PutA flavoenzymes from H. pylori and H. hepaticus revealed that Helicobacter PutA generates reactive oxygen species during proline oxidation by transferring electrons from reduced flavin to molecular oxygen. We further explored the preference for proline as a respiratory substrate and the potential impact of proline metabolism on the redox environment in Helicobacter species during host infection by disrupting the putA gene in H. hepaticus. The resulting putA knockout mutant strain was characterized by oxidative stress analysis and mouse infection studies. The putA mutant strain of H. hepaticus exhibited increased proline levels and resistance to oxidative stress relative to that of the wild-type strain, consistent with proline's role as an antioxidant. The significant increase in stress resistance was attributed to higher proline content, as no upregulation of antioxidant genes was observed for the putA mutant strain. The wild-type and putA mutant H. hepaticus strains displayed similar levels of infection in mice, but in mice challenged with the putA mutant strain, significantly reduced inflammation was observed, suggesting a role for proline metabolism in H. hepaticus pathogenicity in vivo.

APA, Harvard, Vancouver, ISO, and other styles

4

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.

Full text

Abstract:

ABSTRACT Little is known about the molecular pathogenesis of hepatitis and enterocolitis caused by enterohepatic Helicobacter species. Sonicates of the murine pathogen Helicobacter hepaticuswere found to cause progressive cell distension, accumulation of filamentous actin, and G2/M cell cycle arrest in HeLa cell monolayers. The genes encoding this cytotoxic activity were cloned fromH. hepaticus. Three open reading frames with closest homology to cdtA, cdtB, and cdtCfrom Campylobacter jejuni were identified. Sonicates of a laboratory strain of Escherichia coli carrying the clonedcdtABC gene cluster from H. hepaticusreproduced the cytotoxic activities seen with sonicates of H. hepaticus. Cytolethal distending toxin activity is a potential virulence determinant of H. hepaticus that may play a role in the pathogenesis of Helicobacter-associated hepatitis and enterocolitis.

APA, Harvard, Vancouver, ISO, and other styles

5

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.

Full text

Abstract:

ABSTRACT Helicobacter hepaticus infection in A/JCr mice results in chronic active hepatitis characterized by perivascular, periportal, and parenchymal infiltrates of mononuclear and polymorphonuclear cells. This study examined the development of hepatitis and the immune response of A/JCr mice to H. hepaticus infection. The humoral and cell-mediated T helper immune response was profiled by measuring the postinfection (p.i.) antibody response in serum, feces, and bile and by the production of cytokines and proliferative responses by splenic mononuclear cells to H. hepaticusantigens. Secretory immunoglobulin A (IgA) and systemic IgG2a antibody developed by 4 weeks p.i. and persisted through 12 months. Splenocytes from infected mice proliferated and produced more gamma interferon (IFN-γ) than interleukin-4 (IL-4) or IL-5 when cultured with H. hepaticus outer membrane proteins. The predominantly IgG2a antibody response in serum and the in vitro production of IFN-γ in excess of IL-4 or IL-5 are consistent with a Th1 immune response reported in humans and mice infected withHelicobacter pylori and Helicobacter felis, respectively. Mice infected with H. hepaticus developed progressively severe perivascular, periportal, and hepatic parenchymal lesions consisting of lymphohistiocytic and plasmacytic cellular infiltrates. In addition, transmural typhlitis was observed at 12 months p.i. The characterization of a cell-mediated Th1 immune response toH. hepaticus infection in the A/JCr mouse should prove valuable as a model for experimental regimens which manipulate the host response to Helicobacter.

APA, Harvard, Vancouver, ISO, and other styles

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.

Full text

Abstract:

Infection with Helicobacter hepaticus causes chronic active hepatitis in certain strains of mice and is associated with hepatocellular carcinoma in A/JCr mice. Like the gastric helicobacters,H. pylori and H. mustelae, H. hepaticus possesses a high level of urease activity. However, theH. hepaticus urease structural gene sequences have not been previously determined, and the role of the urease enzyme in colonization and in pathogenesis is not known. PCR was used to amplify a portion of the urease structural genes from H. hepaticusgenomic DNA. Amplified DNA fragments were cloned, and the nucleotide sequence was determined. The deduced amino acid sequence of the partialH. hepaticus ureA gene product was found to exhibit 60% identity and 75% similarity to the predicted H. pyloriUreA. The deduced amino acid sequence of a partial H. hepaticus ureB gene product exhibited 75% identity and 87% similarity to the predicted H. pylori UreB. Diversity amongH. hepaticus isolates was evaluated by means of a restriction fragment length polymorphism (RFLP) assay. The 1.6-kb fragments within the ureAB open reading frames, amplified from 11 independent isolates, were digested with the restriction endonuclease HhaI. Three distinct RFLP patterns were observed. Identical RFLP profiles were noted in sequential isolates of one strain of H. hepaticus during an 18 month in vivo colonization study, suggesting that the urease genes ofH. hepaticus are stable. The urease genes amongH. hepaticus strains were also well conserved, showing 98.8 to 99% nucleotide sequence identity among three isolates analyzed. These findings indicate that H. hepaticus has urease structural genes which are homologous to those of the gastric Helicobacter species and that these gene sequences can be used in a PCR and RFLP assay for diagnosis of this important murine pathogen.

APA, Harvard, Vancouver, ISO, and other styles

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.

Full text

Abstract:

ABSTRACT Helicobacter hepaticus causes hepatitis in susceptible strains of mice. Previous studies indicated that A/JCr mice are susceptible and C57BL/6NCr mice are resistant to H. hepaticus-induced hepatitis. We used F1 hybrid mice derived from A/J and C57BL/6 matings to investigate their phenotype and determine their hepatic gene expression profile in response to H. hepaticus infection. F1 hybrid mice, as well as parental A/J and C57BL/6 mice, were divided equally into control and H. hepaticus-infected groups and euthanized at 18 months postinoculation. Hepatic lesions were evaluated histologically and the differential hepatic gene expression in F1 mice was determined by microarray-based global gene expression profiling analysis. H. hepaticus-infected parental strains including A/J and C57BL/6 mice, as well as F1 mice, developed significant hepatitis. Overall, hepatocellular carcinomas or dysplastic liver lesions were observed in 69% of H. hepaticus-infected F1 male mice and H. hepaticus was isolated from hepatic tissues of all F1 mice with liver tumors. Liver tumors, characterized by hepatic steatosis, developed in livers with high hepatitis scores. To identify gene expression specific to H. hepaticus-induced hepatitis and progression to hepatocellular carcinoma in F1 mice, a method using comparative group transcriptome analysis was utilized. The canonical pathway most significantly enriched was immunological disease. Fatty acid synthase and steaoryl-coenzyme A desaturase, the two rate-limiting enzymes in lipogenesis, were upregulated in neoplastic relative to dysplastic livers. This study suggests a synergistic interaction between hepatic steatosis and infectious hepatitis leading to hepatocellular carcinoma. The use of AB6F1 and B6AF1 mice, as well as genetically engineered mice, on a C57BL/6 background will allow studies investigating the role of chronic microbial hepatitis and steatohepatitis in the pathogenesis of liver cancer.

APA, Harvard, Vancouver, ISO, and other styles

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.

Full text

Abstract:

Enterohepatic Helicobacters, such as Helicobacter hepaticus and Helicobacter pullorum, are associated with several intestinal and hepatic diseases. Their main virulence factor is the cytolethal distending toxin (CDT). In the present study, whole genome microarray-based identification of differentially expressed genes was performed in vitro in HT-29 intestinal cells while following the ectopic expression of the active CdtB subunit of H. hepaticus CDT. A CdtB-dependent upregulation of the V-maf musculoaponeurotic fibrosarcoma oncogene homolog B (MAFB) gene encoding the MAFB oncoprotein was found, as well as the CdtB-dependent regulation of several MAFB target genes. The transduction and coculture experiments confirmed MAFB mRNA and protein induction in response to CDT and its CdtB subunit in intestinal and hepatic cell lines. An analysis of MAFB protein subcellular localization revealed a strong nuclear and perinuclear localization in the CdtB-distended nuclei in intestinal and hepatic cells. MAFB was also detected at the cell periphery of the CdtB-induced lamellipodia in some cells. The silencing of MAFB changed the cellular response to CDT with the formation of narrower lamellipodia, a reduction of the increase in nucleus size, and the formation of less γH2AX foci, the biomarker for DNA double-strand breaks. Taken together, these data show that the CDT of enterohepatic Helicobacters modulates the expression of the MAFB oncoprotein, which is translocated in the nucleus and is associated with the remodeling of the nuclei and actin cytoskeleton.

APA, Harvard, Vancouver, ISO, and other styles

9

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.

Full text

Abstract:

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.

APA, Harvard, Vancouver, ISO, and other styles

10

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.

Full text

Abstract:

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.

APA, Harvard, Vancouver, ISO, and other styles

11

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.

Full text

Abstract:

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 conditions or colonized with H. hepaticus; both groups were exposed to asphyxia and cold stress. The incidence of NEC, expression of Toll-like receptors (TLRs), production of cytokines and mucins, and presence of autophagy regulators were evaluated at the site of injury. H. hepaticus infection increased the incidence of NEC from 39 to 71% and significantly increased levels of TLR4 receptor, expression of proinflammatory cytokines CXCL1, IL-1β, IL-12, and IL-23, and altered activation of autophagy. H. hepaticus induces inflammation and increases the incidence and severity of experimental NEC; this is consistent with observations in neonates of blooms of proinflammatory microbes just before the onset of NEC. Future studies using rodent NEC models should include testing for H. hepaticus infection. Further studies in neonates of early identification and/or diminution of proinflammatory microbes may be beneficial in decreasing the incidence of NEC.

APA, Harvard, Vancouver, ISO, and other styles

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.

Full text

Abstract:

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.

APA, Harvard, Vancouver, ISO, and other styles

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.

Full text

Abstract:

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, including the urea transporter gene ureI. Downstream genes were homologs of the nik nickel transport operon of E. coli. Nongastric H. hepaticusproduces urease similar to that of H. pylori.

APA, Harvard, Vancouver, ISO, and other styles

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.

Full text

Abstract:

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. pylori generally contains higher specific activity than H. hepaticus. Wild-type H. hepaticus cells tolerated 6 % O2 for growth, whilst the katA mutant could not survive at this oxygen level. Even at the optimal O2 level, the growth of the H. hepaticus katA strain was severely inhibited, which is also in contrast to H. pylori katA strains. Wild-type H. hepaticus cells withstood exposure to 100 mM H2O2 but the katA mutant cells were killed by the same treatment. Wild-type cells suffered no significant DNA damage by H2O2 treatment (100 mM for 6 min), whilst the same treatment resulted in severe DNA fragmentation in the katA mutant. Thus H. hepaticus KatA plays an important role as an antioxidant protein.

APA, Harvard, Vancouver, ISO, and other styles

15

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.

Full text

Abstract:

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 colonized with stool from SPF mice that harbored or did not harbor endogenous H. hepaticus. After 7 to 9 weeks of colonization, weight loss and mortality were assessed, the colon was isolated for histology and IL-12 secretion, and mesenteric lymph node cells were assessed for T-cell activation markers. It was found that IL-10−/− mice monoassociated with H. hepaticus for up to 16 weeks showed almost no histologic colitis or increased IL-12 production. SPF IL-10-knockout mice had no significant difference in weight loss, mortality rate, histologic scores, colonic IL-12 secretion, or T-cell activation with or withoutH. hepaticus. We conclude that H. hepaticusdoes not induce or potentiate disease in our IL-10−/−mice and therefore is not required to induce colitis in genetically susceptible hosts.

APA, Harvard, Vancouver, ISO, and other styles

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.

Full text

Abstract:

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 of three of five males at 8 wpi and then was eliminated by 16 wpi. Wild-type (WT) H. hepaticus was detected in the corresponding intestinal regions of both male and female mice at 8 and 16 wpi; however, colonization levels of WT H. hepaticus in the cecum and colon of male mice were approximately 1,000-fold higher than in females (P < 0.0079) at 16 wpi. Infection with WT H. hepaticus, but not HhcdtBm7, at 8 wpi was associated with significantly increased mRNA level of ileal and cecal gamma interferon (IFN-γ) in females (P < 0.016 and 0.031 between WT H. hepaticus-infected and sham-dosed females, respectively). In contrast, the mRNA levels of IFN-γ were significantly higher in the colon (P < 0.0079) and trended to be higher in the cecum (P < 0.15) in the HhcdtBm7-colonized male mice versus the sham-dosed controls at 8 wpi. In addition, mRNA levels of ileal IFN-γ were significantly higher in the control females than males at 8 wpi (P < 0.016). There were significantly higher Th1-associated immunoglobulin G2a (IgG2a), Th2-associated IgG1 and mucosal IgA (P < 0.002, 0.002, 0.002, respectively) responses in the mice infected with WT H. hepaticus when compared to HhcdtBm7 at 16 wpi. Colonic interleukin-10 (IL-10) expressions at 16 wpi were significantly lower in both female and male mice colonized by WT H. hepaticus or in males transiently colonized through 8 wpi by HhcdtBm7 versus control mice (P < 0.0159). These lines of evidence indicate that (i) H. hepaticus CDT plays a crucial role in the persistent colonization of H. hepaticus in SW mice; (ii) SW female mice are more resistant to H. hepaticus colonization than male mice; (iii) there was persistent colonization of WT H. hepaticus in cecum, colon, and jejunum but only transient colonization of H. hepaticus in the ileum of female mice; (iv) H. hepaticus colonization was associated with down-regulation of colonic IL-10 production.

APA, Harvard, Vancouver, ISO, and other styles

17

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.

Full text

Abstract:

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 microarray analysis of the wild type versus an isogenic fliA mutant revealed that 11 genes were significantly more highly expressed in wild-type bacteria and 2 genes were significantly more highly expressed in the fliA mutant. Most of these were flagellar genes, but four novel FliA-regulated genes of unknown function were identified. H. hepaticus possesses two identical copies of the gene encoding the FliA-dependent major flagellin subunit FlaA (open reading frames HH1364 and HH1653). We characterized the phenotypes of mutants in which fliA or one or both copies of the flaA gene were knocked out. flaA_1 flaA_2 double mutants and fliA mutants did not synthesize detectable amounts of FlaA and possessed severely truncated flagella. Also, both mutants were nonmotile and unable to colonize mice. Mutants with either flaA gene knocked out produced flagella morphologically similar to those of wild-type bacteria and expressed FlaA and FlaB. flaA_1 mutants which had flagella but displayed reduced motility did not colonize mice, indicating that motility is required for intestinal colonization by H. hepaticus and that the presence of flagella alone is not sufficient.

APA, Harvard, Vancouver, ISO, and other styles

18

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.

Full text

Abstract:

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), and microelectrode measurements on the livers of live mice demonstrated that H2 is available in the host tissue at levels 20-fold greater than the apparent whole-cell Km value.

APA, Harvard, Vancouver, ISO, and other styles

19

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.

Full text

Abstract:

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-type type H. hepaticus developed significant typhlocolitis. However, by 4 months after infection, the CDT-deficient mutant was no longer detectable in IL-10−/− mice, whereas wild-type H. hepaticus persisted for the 8-month duration of the experiment. Animals infected with wild-type H. hepaticus exhibited severe typhlocolitis at 8 months after infection, while animals originally challenged with the CDT-deficient mutant had minimal cecal inflammation at this time point. In follow-up experiments, animals that cleared infection with the CDT-deficient mutant were protected from rechallenge with either mutant or wild-type H. hepaticus. Animals infected with wild-type H. hepaticus developed serum immunoglobulin G1 (IgG1) and IgG2c responses against H. hepaticus, while animals challenged with the CDT-deficient mutant developed significantly lower IgG2c responses and failed to mount IgG1 responses against H. hepaticus. These results suggest that CDT plays a key immunomodulatory role that allows persistence of H. hepaticus and that in IL-10−/− mice this alteration of the host immune response results in the development of colitis.

APA, Harvard, Vancouver, ISO, and other styles

20

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.

Full text

Abstract:

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, which allows this pathogen to induce or contribute to chronic inflammatory disease. We demonstrated in the present study that the innate immune responses of intestinal epithelial cells to lipopolysaccharide (LPS) via Toll-like receptor 4 (TLR4) and to flagellin-mediated activation via TLR5 are reduced by H. hepaticus infection through soluble bacterial factors. In particular, H. hepaticus lysate and the soluble component LPS antagonized TLR4- and TLR5-mediated immune responses of intestinal epithelial cells. H. hepaticus lysate and LPS inhibited development of endotoxin tolerance to Escherichia coli LPS. Suppression of innate immune responses by H. hepaticus LPS thus may affect intestinal responses to the resident microbial flora, epithelial homeostasis, and intestinal inflammatory conditions.

APA, Harvard, Vancouver, ISO, and other styles

21

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.

Full text

Abstract:

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 be susceptible to Helicobacter hepaticus-induced liver tumours. Sixteen mice served as mock-dosed controls. At 6, 12 and 18 months post-inoculation (p.i.), there were statistically significant (P<0.05) differences in mean inflammation scores for the caecum and proximal colon between experimentally infected and control mice. Differences in hepatic inflammation were significant (P<0.05) at 6 and 12 months p.i. between the two groups but not at the 18 month time point. Two infected male mice had livers with severe hepatitis, and the liver samples were culture positive for H. marmotae. Serum IgG levels in the mice dosed with H. marmotae were elevated for the duration of the study. These results demonstrate that the woodchuck helicobacter can successfully colonize mice and cause enterohepatic disease. In the future, a mouse-adapted strain of H. marmotae could be selected to maximize colonization and lesion development. Such a woodchuck helicobacter-infected mouse model could be used to dissect potential mechanisms of microbial co-carcinogenesis involved in tumour development in woodchucks with WHV and in humans with hepatitis B virus.

APA, Harvard, Vancouver, ISO, and other styles

22

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.

Full text

Abstract:

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 granulating cytotoxin in H. hepaticus. Challenge of C57BL/6 interleukin 10−/− mice with isogenic H. hepaticus mutants revealed that CDT expression is not required for colonization of the murine gut. However, a CDT-negative H. hepaticus mutant had a significantly diminished capacity to induce lesions in this murine model of inflammatory bowel disease.

APA, Harvard, Vancouver, ISO, and other styles

23

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.

Full text

Abstract:

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.

APA, Harvard, Vancouver, ISO, and other styles

24

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.

Full text

Abstract:

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. hepaticus was detected in the gallbladder, bile ducts, and liver by PCR, as well as the number of bacteria present in the liver, tended to increase with increasing age and longer infection time. Anti-H. hepaticus immunoglobulin G antibodies were positive by enzyme-linked immunosorbent assay only in inoculated mice. Pathological findings were also more frequent as the mice grew older: fibrosis was present (especially in the peripheral part of the liver), and significant portal inflammation including lymphoid nodules was present in almost all infected animals. Biliary lesions of neutrophilic acute cholangitis or lymphocytic cholangitis were noted. However, lesions were also observed in uninfected animals, although at a significantly lower level, and the only hepatocellular carcinoma occurred in an uninfected mouse. The evolution towards hepatocarcinoma is not always the endpoint and may depend on the bacterial strain and on the environmental conditions.

APA, Harvard, Vancouver, ISO, and other styles

25

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.

Full text

Abstract:

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 gene and Cyp4a protein expression. Castrated males and those receiving the competitive androgen receptor antagonist flutamide had significantly less severe hepatitis as determined by histologic activity index than intact controls at 4 months. Importantly, the powerful androgen receptor agonist dihydrotestosterone did not promote hepatitis. No effect on hepatitis was evident in males treated with the 5α-reductase inhibitor dutasteride, the peroxisome proliferator-activated receptor-α agonist bezafibrate, or the nonsteroidal anti-inflammatory drug flufenamic acid. Consistent with previous observations of hepatitis-associated liver-gender disruption, transcriptional alterations involved both feminine (cytochrome P450 4a14) and masculine (cytochrome P450 4a12 and trefoil factor 3) genes, as well gender-neutral (H19 fetal liver mRNA, lipocalin 2, and ubiquitin D) genes. Hepatitis was associated with increased unsaturated C18 long-chain fatty acids (oleic acid and linoleic acid) relative to saturated stearic acid. Our results indicate that certain forms of androgen interruption can inhibit H. hepaticus-induced hepatitis in young male mice, whereas androgen receptor agonism does not worsen disease. This raises the possibility of targeted hormonal therapy in young male patients with childhood-acquired HBV.

APA, Harvard, Vancouver, ISO, and other styles

26

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.

Full text

Abstract:

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.

APA, Harvard, Vancouver, ISO, and other styles

27

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.

Full text

Abstract:

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 and intestinal tumorigenesis, the immunodeficient compound mutant strain BALB-RagMin (C.Cg-Rag2 −/− Apc Min/+) was generated. BALB-RagMin mice had a significant increase in tumors in the small, but not large, intestine relative to their BALB-Min counterparts (43.0 versus 24.0 tumors/mouse, respectively). The results suggest that the adaptive immune system plays a role in either the elimination or the equilibrium phase of cancer immunoediting in the small intestine in this model. We investigated the effect of the enterohepatic bacterial pathogen Helicobacter hepaticus on liver and intestine tumorigenesis in BALB-RagMin mice. H. hepaticus-infected BALB-RagMin mice developed moderate hepatitis, moderate typhlitis, and mild colitis. There were no differences in small intestine and cecal tumor multiplicity, regionality, or size relative to that in uninfected mice. However, H. hepaticus-infected BALB-RagMin mice had a significant increase in colon tumor incidence relative to uninfected BALB-RagMin mice (23.5% versus 1.7%, respectively). The data suggest that H. hepaticus, which is present in many research colonies, promotes colon tumorigenesis in the BALB-RagMin mouse and that it has the potential to confound colon tumorigenesis studies.

APA, Harvard, Vancouver, ISO, and other styles

28

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.

Full text

Abstract:

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 were treated with probiotic Lactobacillus reuteri in combination with Lactobacillus paracasei and then challenged with H. hepaticus. Ten weeks postinoculation, the severity of typhlocolitis was assessed by histologic examination of the cecocolic region. Intestinal proinflammatory cytokine responses were evaluated by real-time quantitative reverse transcriptase PCR and immunoassays, and the quantities of intestinal H. hepaticus were evaluated by real-time PCR. Intestinal colonization by TNF-α-inhibitory lactobacilli reduced intestinal inflammation in H. hepaticus-challenged IL-10-deficient mice despite similar quantities of H. hepaticus in cocolonized animals. Proinflammatory colonic cytokine (TNF-α and IL-12) levels were lowered in Lactobacillus-treated animals. In this H. hepaticus-challenged IL-10-deficient murine colitis model, lactobacilli demonstrated probiotic effects by direct modulation of mucosal inflammatory responses.

APA, Harvard, Vancouver, ISO, and other styles

29

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.

Full text

Abstract:

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 the dominant member of the community. Colonization of the mucosa by H. hepaticus was associated with a decrease in the overall diversity of the microbial community, in large part due to changes in evenness resulting from the relative dominance of H. hepaticus as a member of the community. Our results demonstrate that invasion of the complex gastrointestinal microbial community by a pathogenic microorganism causes reproducible and significant disturbances in the community structure. The use of non-culture-based methods to monitor these changes should lead to a greater understanding of the ecological principles that govern pathogen invasion and may lead to novel methods for the prevention and control of gastrointestinal pathogens.

APA, Harvard, Vancouver, ISO, and other styles

30

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.

Full text

APA, Harvard, Vancouver, ISO, and other styles

31

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.

Full text

Abstract:

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.

APA, Harvard, Vancouver, ISO, and other styles

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.

Full text

Abstract:

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 proteins and ureA mRNA. Insertional inactivation of the fur gene abolished iron-responsive repression of urease activity, whereas inactivation of the perR gene did not affect iron-responsive regulation of urease activity. The iron-responsive promoter element was identified directly upstream of the H. hepaticus ureA gene. Recombinant H. hepaticus Fur protein bound to this ureA promoter region in a metal-dependent matter, and binding resulted in the protection of a 41-bp, Fur box-containing operator sequence located at positions −35 to −75 upstream of the transcription start site. In conclusion, H. hepaticus Fur controls urease expression at the transcriptional level in response to iron availability. This represents a novel type of urease regulation in ureolytic bacteria and extends the already diverse regulatory repertoire of the Fur protein.

APA, Harvard, Vancouver, ISO, and other styles

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.

Full text

Abstract:

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− subpopulations of these cells, their frequency being higher in the latter. The mechanism by which CD25+ and CD25− CD45RBlow CD4+ cells block colitis involves IL-10 and not transforming growth factor (TGF)-β, as treatment with anti–IL-10R but not anti–TGF-β monoclonal antibody abrogated their protective effect. In vitro, CD45RBlow CD4+ cells from infected WT mice were shown to produce IL-10 and suppress interferon-γ production by IL-10 KO CD4+ cells in an H. hepaticus antigen–specific manner. Together, our data support the concept that H. hepaticus infection results in the induction in WT mice of regulatory T cells that prevent bacteria-induced colitis. The induction of such cells in response to gut flora may be a mechanism protecting normal individuals against inflammatory bowel disease.

APA, Harvard, Vancouver, ISO, and other styles

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.

Full text

Abstract:

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.

APA, Harvard, Vancouver, ISO, and other styles

35

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.

Full text

APA, Harvard, Vancouver, ISO, and other styles

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.

Full text

APA, Harvard, Vancouver, ISO, and other styles

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.

Full text

Abstract:

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.

APA, Harvard, Vancouver, ISO, and other styles

38

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.

Full text

Abstract:

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 hepatitis and hepatocellular carcinoma. Rodent models enhance our understanding of infectious cancer pathogenesis and suggest novel targets for intervention.

APA, Harvard, Vancouver, ISO, and other styles

39

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.

Full text

APA, Harvard, Vancouver, ISO, and other styles

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.

Full text

Abstract:

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 various research and vendor facilities. Further studies are necessary to define its association with disease and other microbiota in hamsters, as well as its impact on research projects involving hamsters. H. aurati (GenBank accession number AF297868) can be used in animal experiments to define the factors that are important for gastric helicobacter pathogenesis.

APA, Harvard, Vancouver, ISO, and other styles

41

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.

Full text

Abstract:

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. In a 5-h period, the extent of 14C-labeled amino acid uptake by the wild type was markedly enhanced in the presence of hydrogen and was >5-fold greater than that of the hyaB mutant strain. In the presence of H2, the short-term whole-cell amino acid uptake V max of the parent strain was about 2.2-fold greater than for the mutant, but the half-saturation affinity for amino acid transport was the same for the parent and mutant strain. The liver- and cecum-colonizing abilities of the strains was estimated by real-time PCR quantitation of the H. hepaticus-specific cytolethal distending toxin gene and showed similar animal colonization for the hyaB mutant and the wild type. However, at 21 weeks postinoculation, the livers from mice inoculated with wild type exhibited moderate lobular lymphoplasmacytic hepatitis with hepatocytic coagulative necrosis, but the hydrogenase mutants exhibited no histological evidence of lobular inflammation or necrosis.

APA, Harvard, Vancouver, ISO, and other styles

42

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.

Full text

APA, Harvard, Vancouver, ISO, and other styles

43

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.

Full text

APA, Harvard, Vancouver, ISO, and other styles

44

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.

Full text

APA, Harvard, Vancouver, ISO, and other styles

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.

Full text

APA, Harvard, Vancouver, ISO, and other styles

46

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.

Full text

APA, Harvard, Vancouver, ISO, and other styles

47

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.

Full text

APA, Harvard, Vancouver, ISO, and other styles

48

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.

Full text

APA, Harvard, Vancouver, ISO, and other styles

49

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.

Full text

APA, Harvard, Vancouver, ISO, and other styles

50

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.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Journal articles on the topic 'Helicobacter hepaticus'

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles