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PubMed2000

Serum antibodies to Helicobacter hepaticus and Helicobacter pylori in patients with chronic liver disease.

BACKGROUND: Bile tolerant helicobacter species such as H hepaticus and H bilis have frequently been reported to cause hepatitis in mice and other rodents. AIMS: To investigate the possible pathogenic role of these and other helicobacter species in chronic liver disease in humans. METHODS: Serum samples from 144 patients with various chronic liver diseases, 30 patients with primary sclerosing cholangitis (PSC), and 48 healthy blood donors were analysed for antibodies against H hepaticus murine strain CCUG 33637 and H pylori strain CCUG 17874. Cell surface proteins of H hepaticus were extracted by acid glycine buffer and used in an enzyme immunoassay (EIA) and immunoblot (IB). RESULTS: 56 of 144 (39%) patients with chronic liver diseases and six of 30 (20%) with PSC showed increased antibody concentrations in the H hepaticus EIA; in the H pylori EIA the numbers were 58% and 13% respectively. Compared with the healthy blood donors the antibody reactivity against the two helicobacter species was not increased (46% and 48% respectively). Patient serum samples retested by the H hepaticus EIA after absorption with sonicated H pylori cells remained positive in 12 of 37 (33%) serum samples. Distinct antibody reactivity to 55-65 kDa proteins was observed by H hepaticus IB, after the absorption step, and was considered specific for H hepaticus. These 12 serum samples were from patients with chronic alcoholic liver disease. CONCLUSIONS: Antibodies to H hepaticus, often cross reacting with H pylori, occur frequently in patients with chronic liver diseases, with no clear cut relation to specific diagnostic groups. The pathogenic significance of these findings is not known.

Adult↗
PubMed1995

MALToma-like lesions in the murine gastric mucosa after long-term infection with Helicobacter felis. A mouse model of Helicobacter pylori-induced gastric lymphoma.

The long-term consequences of helicobacter infection were observed in an established murine model of human helicobacter infection. Stomachs of specific pathogen-free BALB/c mice infected with Helicobacter felis were examined for inflammation with particular reference to lymphoid cell proliferation and lymphoepithelial lesions. There was little evidence of an inflammatory response in animals sacrificed up to 19 months after infection. In contrast, from 22 months, 38% of infected animals had lymphoid follicles, whereas no lymphoid follicles were found in noninfected control animals. Lymphoepithelial lesions were observed in 25% of infected mice compared with none in controls. Immunostaining confirmed the B-cell nature of the lymphoid infiltrate. The morphology of these lesions closely resemble those seen in human gastric MALToma. This animal model would provide an opportunity to study the pathogenesis of lymphoproliferative disease.

Animals↗
PubMed1991

Phylogeny of Helicobacter felis sp. nov., Helicobacter mustelae, and related bacteria.

Strain CS1T (T = type strain) is a gram-negative, microaerophilic, urease-positive, spiral-shaped bacterium that was isolated from the gastric mucosa of a cat. Additional strains which possessed biochemical and ultrastructural characteristics similar to those of strain CS1T were isolated from the gastric mucosa of cats and dogs. The guanine-plus-cytosine content of the DNA of strain CS1T was 42.5 mol%. The 16S rRNA sequences of strain CS1T, strain DS3 (a spiral-shaped isolate from a dog), and Helicobacter mustelae were determined by direct RNA sequencing, using a modified Sanger method. These sequences were compared with the 16S rRNA sequences of Helicobacter pylori, "Flexispira rappini," Wolinella succinogenes, and 11 species of campylobacters. A dendrogram was constructed based upon sequence similarities. Strains CS1T and DS3 were very closely related (level of similarity, 99.3%). Two major phylogenetic groups were formed; one group consisted of strains CS1T and DS3, H. mustelae, H. pylori, "F. rappini," and W. succinogenes, and the other group contained the true campylobacters. The average level of similarity between members of these two groups was 84.9%. Within the first group, strains CS1T and DS3, H. pylori, and H. mustelae formed a cluster of organisms with an interspecies similarity level of 94.5%. The phylogenetic positions of W. succinogenes and "F. rappini" were just outside this cluster. On the basis of the results of this study, we believe that strains CS1T (= ATCC 49179T) and DS3 represent a new species of the genus Helicobacter, for which we propose the name Helicobacter felis.

Animals↗
PubMed2002

A placebo-controlled randomized trial of eradication of Helicobacter pylori in the general population: study design and response rates of the Bristol Helicobacter Project.

The Bristol Helicobacter Project is an ongoing, pragmatic, double-blind placebo-controlled trial of the effect of Helicobacter pylori eradication on symptoms of dyspepsia, health utilization and costs, and quality of life in the adult population. Commencing in 1996, 27,536 individuals ages 20-59 years who were registered with seven primary care centers in Bristol and the surrounding areas in southwest England were invited to undergo a 13C urea breath test. There was no selection on the basis of symptoms and 23.5% had dyspepsia on entry to the study. A total of 10,537 people were tested (38.3% of those invited), 1636 tested positive (15.5% of those tested), and 1558 (95.2% of those who tested positive) were randomized to H. pylori eradication therapy or placebo. The rate of participation in the screening phase increased with age (odds ratio [OR]: 1.42 per decade, 95% CI: 1.31 to 1.54) and female gender (OR: 1.35, 95% CI: 1.27 to 1.43) but decreased with lower socioeconomic status (OR: 0.70, 95% CI: 0.56 to 0.86 comparing lowest with highest category). H. pylori prevalence increased with age (OR: 1.69 per decade, 95% CI: 1.51 to 1.89) and lower socioeconomic status (OR: 1.33, 95% CI: 1.05 to 1.69) but was lower in women (OR: 0.87, 95% CI: 0.76 to 1.00). Population-based trials of H. pylori eradication are feasible but necessitate screening large numbers of people to identify those who are infected and who may benefit from eradication. In the Bristol Helicobacter Project the rate of participation varied inversely with both social deprivation and the prevalence of the infection.

Adult↗
PubMed2002

Molecular microbiology and pathogenesis of Helicobacter and Campylobacter updated: a meeting report of the 11th conference on Campylobacter, Helicobacter and related organisms.

The genome analysis of the gastrointestinal pathogens Helicobacter and Campylobacter has stimulated a wealth of new research activities, which are presented every 2 years at the international conferences on Campylobacter, Helicobacter and Related Organisms (CHRO). Both organisms represent excellent models for the identification of new molecular mechanisms involved in pathogenesis, host response and physiological adaptation in course of acute and chronic infectious diseases. The investigation of their global distribution, pronounced genetic and antigenic diversity as well as the molecular mechanisms allowing long-term persistence in hostile and unusual microbial habitats, is a challenge for scientists of many different disciplines world-wide. With a focus on the molecular microbiology aspects, this review summarizes recent trends in Helicobacter and Campylobacter research by highlighting selected presentations at the 11th CHRO conference. The topics include the discovery of new virulence factors, functional analysis of protein secretion systems, host signalling pathways, adaptation to stress conditions, global gene regulation, and genetic variability.

Animals↗
PubMed1999

Effect of processed and non-processed coffee samples on gastric potential difference. Study with healthy male Helicobacter pylori-positive and Helicobacter pylori-negative volunteers.

In an open trial with 18 healthy male volunteers (21-45 years old) the effect of processed (test) and non-processed (reference) coffee samples of same origin on the gastric potential difference (GPD) was studied. Test coffee samples were processed with the patented "Darboven improvement procedure" before roasting. All treatment groups were subdivided according to the Helicobacter pylori status of the volunteers. The evaluation of the target parameters Reizindex (RI), area under the baseline (AUB), maximum potential difference (Pdmax) and total time (ttot) revealed a significant lower RI (p = 0.0282) and AUB (p = 0.0136), and a significant shorter ttot (p = 0.0286) for the processed coffee. Total cholesterol, high-density lipoprotein (HDL) cholesterol, and pancreatic peptides showed a comparable marked increase of the arithmetic mean with both coffee samples, however, being more intense in the Helicobacter pylori-positive subgroup than in the Helicobacter pylori-negative subgroup. No negative findings concerning tolerability and safety could be seen. In conclusion, the test coffee samples processed with a new method to improve the stomach mucosal irritation-potential of coffee charges revealed a remarkably lower stomach mucosal irritation.

Adult↗
PubMed1998

Inhibition of Helicobacter pylori and Helicobacter mustelae binding to lipid receptors by bovine colostrum.

Helicobacter pylori, the etiologic agent of chronic-active gastritis and duodenal ulcers in humans, and Helicobacter mustelae, a gastric pathogen in ferrets, bind to phosphatidylethanolamine (PE), a constituent of host gastric mucosal cells, and to gangliotetraosylceramide (Gg4) and gangliotriaosylceramide (Gg3). The effect of a bovine colostrum concentrate (BCC) on the interaction of H. pylori and H. mustelae to their lipid receptors was examined. BCC blocked attachment of both species to Gg4, Gg3, and PE. Partial inhibition of binding was observed with native bovine and human colostra. BCC lacked detectable antibodies (by immunoblotting) to H. pylori surface proteins (adhesins). However, colostral lipid extracts contained PE and lyso-PE that bound H. pylori in vitro. These results indicate that colostrum can block the binding of Helicobacter species to select lipids and that binding inhibition is conferred, in part, by colostral PE or PE derivatives. Colostral lipids may modulate the interaction of H. pylori and other adhesin-expressing pathogens with their target tissues.

Adhesins, Bacterial↗
PubMed1999

Genetic diversity of canine gastric helicobacters, Helicobacter bizzozeronii and H. salomonis studied by pulsed-field gel electrophoresis.

Genetic diversity of Helicobacter bizzozeronii and H. salomonis, two recently identified canine gastric Helicobacter spp., was studied by pulsed-field gel electrophoresis (PFGE). All 15 Finnish H. bizzozeronii strains collected between 1991 and 1996 from pet dogs produced different PFGE patterns with all restriction endonucleases studied (AscI, ApaI, SpeI, NotI and PacI) suggesting significant genetic diversity. The five independent H. salomonis strains produced four different patterns with these enzymes; two strains showed identical patterns with all the enzymes. Three separate isolates from one dog had identical patterns, suggesting long-lasting infection with the same strain. H. salomonis strains had several small fragments common for all strains, suggesting relatedness. The PFGE method was shown to be useful for epidemiological studies of canine gastric helicobacter infection. Hybridisation of the DNA digests with digoxigenin-labelled ureB or 16S rRNA gene probes generated by PCR indicated conservation in the localisation of these genes in the H. salomonis genome, because the probes hybridised with similar size fragments of different strains. In contrast, the probes hybridised with different size fragments of H. bizzozeronii strains. Comparison of Southern blots of PFGE patterns digested with SpeI, ApaI and AscI indicated that each species has two 16S rRNA genes and one urease gene. Genome sizes of 11 H. bizzozeronii strains estimated from SpeI and NotI patterns were c. 1.6-1.9 Mb and those of five H. salomonis strains estimated from NotI and PacI patterns were c. 1.7-1.8 Mb.

Animals↗
PubMed1994

Non-motile mutants of Helicobacter pylori and Helicobacter mustelae defective in flagellar hook production.

Flagellar hooks were purified from Helicobacter pylori and Helicobacter mustelae. The 70 x 16 nm H. pylori hook was composed of FlgE subunits of 78kDa, while the 72 x 16 nm H. mustelae hook was composed of 87 kDa subunits. N-terminal sequence was obtained for the FlgE proteins of both species, and for an internal H. mustelae FlgE peptide. Degenerate oligonucleotide primers allowed amplification of a 1.2 kb fragment from the H. mustelae chromosome, which carried part of the flgE gene. The corresponding H. pylori gene was cloned by immunoscreening of a genomic library constructed in lambda ZAP Express. The translated H. pylori flgE sequence indicated a protein with limited homology with the hook proteins from Salmonella typhimurium and Treponema phagedenis. Mutants of H. pylori and H. mustelae defective in hook production generated by allele replacement were non-motile and devoid of flagellar filaments but produced both flagellin subunits, which were localized in the soluble fraction of the cell. The level of flagellin production was unchanged in the mutants, indicating that the regulation of flagellin expression in Helicobacter differs from that in the Enterobacteriaceae.

Amino Acid Sequence↗
PubMed1992

Helicobacter mustelae isolation from feces of ferrets: evidence to support fecal-oral transmission of a gastric Helicobacter.

Helicobacter mustelae has been isolated from stomachs of ferrets with chronic gastritis and ulcers. When H. mustelae is inoculated orally into H. mustelae-negative ferrets, the animals become colonized and develop gastritis, a significant immune response, and a transient hypochlorhydria. All of these features mimic Helicobacter pylori-induced gastric disease in humans. Because the epidemiology of H. pylori infection is poorly understood and its route of transmission is unknown, the feces of weanling and adult ferrets were cultured for the presence of H. mustelae. H. mustelae was isolated from the feces of 11 of 36 ferrets by using standard helicobacter isolation techniques. H. mustelae was identified by biochemical tests, ultrastructural morphology, reactivity with specific DNA probes, and 16S rRNA sequencing. H. mustelae was not recovered from 20-week-old ferrets which had been H. mustelae positive as weanlings, nor was H. mustelae recovered from 1-year-old ferrets. Isolation of H. mustelae from feces may correspond to periods of transient hypochlorhydria, or H. mustelae may be shed in feces intermittently. The H. mustelae-colonized ferret provides an ideal model for studying the pathogenesis and transmission of H. pylori-induced gastric disease.

Animals↗
PubMed1993

Helicobacter mustelae and Helicobacter pylori bind to common lipid receptors in vitro.

Helicobacter pylori is a recently recognized human pathogen causing chronic-active gastritis in association with duodenal ulcers and gastric cancer. Helicobacter mustelae is a closely related bacterium with similar biochemical and morphologic characteristics. H. mustelae infection of antral and fundic mucosa in adult ferrets causes chronic gastritis. An essential virulence property of both Helicobacter species is bacterial adhesion to mucosal surfaces. The aim of this study was to determine whether H. mustelae binds to the same lipids shown previously to be receptors for H. pylori adhesion in vitro. By using thin-layer chromatography overlay and a receptor-based enzyme-linked immunosorbent assay, H. mustelae was found to bind the same receptor lipids as H. pylori, namely, phosphatidylethanolamine and gangliotetraosylceramide. In addition, both H. pylori and H. mustelae bound to a deacylplasmalogen phosphatidylethanolamine. In contrast to H. pylori, H. mustelae binding to receptors was unaffected by motility or viability. Murine monoclonal and bovine polyclonal antibodies against exoenzyme S, and exoenzyme S itself (from Pseudomonas aeruginosa), inhibited binding of H. mustelae to phosphatidylethanolamine and gangliotetraosylceramide. These findings show that H. mustelae binds in vitro to the same lipid receptors as H. pylori and suggest that the adhesion of H. mustelae to such species is mediated by preformed, surface-exposed adhesins which include an exoenzyme S-like protein.

ADP Ribose Transferases↗
PubMed1995

Protein Hpn: cloning and characterization of a histidine-rich metal-binding polypeptide in Helicobacter pylori and Helicobacter mustelae.

Helicobacter pylori is a human gastrointestinal pathogen involved in gastritis, duodenal ulcers, and gastric neoplasia. This microorganism produces large amounts of a urease which, like all known ureases, has nickel in the active site. We have identified a protein in clinical isolates of H. pylori and an identical protein in the ferret pathogen Helicobacter mustelae that strongly binds Ni2+ and Zn2+. This protein has been named Hpn to emphasize its origins in H. pylori and its affinity for nickel. The encoding hpn gene, cloned and expressed in Escherichia coli ER1793, has an open reading frame (180 bp) that specifies a protein with a calculated molecular mass of 7,077 Da and with the same amino-terminal sequence as that of wild-type Hpn. The deduced sequence of Hpn consists of 60 amino acids, of which 28 (47%) are histidines. The hpn gene does not map with the urease gene cluster on the H. pylori chromosome. An Hpn-negative, isogenic H. pylori strain, generated by hpn gene deletion and grown on blood agar, had the same urease activity that wild-type cells did. Thus, the role of Hpn in helicobacters is unknown.

Amino Acid Sequence↗
PubMed1993

Cloning and genetic characterization of the Helicobacter pylori and Helicobacter mustelae flaB flagellin genes and construction of H. pylori flaA- and flaB-negative mutants by electroporation-mediated allelic exchange.

Helicobacter pylori is one of the most common human pathogens. It causes chronic gastritis and is involved in the pathogenesis of gastroduodenal ulcer disease and possibly gastric carcinoma. Helicobacter mustelae is a bacterium closely related to H. pylori that causes gastritis and ulcer disease in ferrets and is therefore considered an important animal model of gastric Helicobacter infections. Motility, even in a viscous environment, is conferred to the bacteria by several sheathed flagella and is regarded as one of their principal virulence factors. The flagellar filament of H. pylori consists of two different flagellin species expressed in different amounts. The gene (flaA) encoding the major flagellin has recently been cloned and sequenced. Here we report the cloning and sequencing of two highly homologous new flagellin genes from H. pylori 85P and H. mustelae NCTC 12032. The nucleotide sequence of the H. pylori gene proved that it encoded the second flagellin molecule found in H. pylori flagellar filaments. The genes were named flaB. The H. mustelae and H. pylori flaB genes both coded for proteins with 514 amino acids and molecular masses of 54.0 and 53.9 kDa, respectively. The proteins shared 81.7% identical amino acids. The degree of conservation between H. pylori FlaB and the H. pylori FlaA major flagellin was much lower (58%). Both flaB genes were preceded by sigma 54-like promoter sequences. Mapping of the transcription start site for the H. pylori flaB gene by a primer extension experiment confirmed the functional activity of the sigma 54 promoter. To evaluate the importance of both genes for motility, flaA- and flaB-disrupted mutants of H. pylori N6 were constructed by electroporation-mediated allelic exchange and characterized by Western blot (immunoblot) analysis and motility testing. Both mutations selectively abolished the expression of the targeted gene without affecting the synthesis of the other flagellin molecule. Whereas flaA mutants were completely nonmotile, flaB mutants retained motility.

Amino Acid Sequence↗
PubMed2004

Helicobacter acinonychis: genetic and rodent infection studies of a Helicobacter pylori-like gastric pathogen of cheetahs and other big cats.

Insights into bacterium-host interactions and genome evolution can emerge from comparisons among related species. Here we studied Helicobacter acinonychis (formerly H. acinonyx), a species closely related to the human gastric pathogen Helicobacter pylori. Two groups of strains were identified by randomly amplified polymorphic DNA fingerprinting and gene sequencing: one group from six cheetahs in a U.S. zoo and two lions in a European circus, and the other group from a tiger and a lion-tiger hybrid in the same circus. PCR and DNA sequencing showed that each strain lacked the cag pathogenicity island and contained a degenerate vacuolating cytotoxin (vacA) gene. Analyses of nine other genes (glmM, recA, hp519, glr, cysS, ppa, flaB, flaA, and atpA) revealed a approximately 2% base substitution difference, on average, between the two H. acinonychis groups and a approximately 8% difference between these genes and their homologs in H. pylori reference strains such as 26695. H. acinonychis derivatives that could chronically infect mice were selected and were found to be capable of persistent mixed infection with certain H. pylori strains. Several variants, due variously to recombination or new mutation, were found after 2 months of mixed infection. H. acinonychis ' modest genetic distance from H. pylori, its ability to infect mice, and its ability to coexist and recombine with certain H. pylori strains in vivo should be useful in studies of Helicobacter infection and virulence mechanisms and studies of genome evolution.

Acinonyx↗
PubMed2002

Two decades of Helicobacter pylori: a review of the Fourth Western Pacific Helicobacter Congress.

From March 3 to 6, 2002, Helicobacter enthusiasts gathered in Perth, Australia for the Fourth Western Pacific Helicobacter Congress to celebrate the 20th anniversary of the modern discovery of this organism by Barry Marshall and Robin Warren. The meeting included state-of-the-art lectures highlighting the breakthroughs that have occurred since the discovery of this bacterium. As well, advances from the forefront of current Helicobacter pylori research were presented, particularly in the realm of genomics and molecular biology. A symposium about vaccines and trends for future H pylori research completed this congress. The purpose of the present review is to summarize the highlights from this conference, emphasizing new advances.

Animals↗
PubMed1995

Lipid profiles of Helicobacter pylori and Helicobacter mustelae grown in serum-supplemented and serum-free media.

Many of Helicobacter species have been found to have novel cholesteryl glucosides (CGs). To study the biosynthetic mechanism of CGs, the lipid profiles of H. pylori and H. mustelae grown in serum-supplemented and cholesterol-restricted serum-free media were investigated. In contrast to the serum-supplemented state, helicobacters had less CGs in the serum-free state; a trace amount of CGs and no CG was detected in H. pylori and H. mustelae, respectively. The proportion of total and individual phospholipid also showed significant alteration. Unknown lipids which did not contain phosphate and sugar were detected in the serum-free state, but not in the serum-supplemented state. The CGs were found to be distributed mainly in the membrane fractions, and one of the unknown lipids was found exclusively in the cytosol fraction. Based on these data, it is apparent that the CGs of helicobacters are synthesized by de novo uptake of cholesterol from the media. The unknown lipids detected in the serum-free state may be storage lipids, appearing in response to depletion of nutrients, especially cholesterol, or other factors in the media.

Culture Media↗
PubMed2002

Helicobacter muricola sp. nov., a novel Helicobacter species isolated from the ceca and feces of Korean wild mouse (Mus musculus molossinus).

A slowly growing microaerophilic Helicobacter strain was isolated from the ceca and fecal pellets of Korean wild mice (Mus musculus molossinus). This bacterial strain possessed a pair of nonsheathed bipolar flagella, was positive for urease, catalase and oxidase, and reduced nitrate to nitrite. It proved susceptible to nalidixic acid and resistant to cephalodine, and did not hydrolyze hippurate. On the basis of phenotypic characteristics and 16S rRNA gene sequence analysis, the isolate represents a new species of the genus Helicobacter, for which the name Helicobacter muricola sp. nov. is proposed; the type strain of the new species is w-06T.

Animals↗
PubMed1996

Isolation of a novel Helicobacter species, Helicobacter cholecystus sp. nov., from the gallbladders of Syrian hamsters with cholangiofibrosis and centrilobular pancreatitis.

A filamentous, gram-negative, motile bacterium with a single polar sheathed flagellum was isolated from gallbladders of hamsters with cholangiofibrosis and centrilobular pancreatitis. Bacteria grew under microaerophilic conditions at 37 and 42 degrees C, were oxidase, catalase, arginine aminopeptidase, and L-arginine arylamidase positive, reduced nitrate to nitrite, were resistant to cephalothin, and exhibited intermediate susceptibility to nalidixic acid. Sequence analysis of the 16S rRNA gene indicated that the bacterium was a novel member of the Helicobacter genus, most closely related to Helicobacter pametensis. We propose to name this bacterium Helicobacter cholecystus. In epidemiologic studies, isolation of H. cholecystus correlated strongly with the presence of cholangiofibrosis and centrilobular pancreatitis; however, further studies are needed to define the role of this bacterium in pathogenesis.

Animals↗