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PubMed1997

Helicobacter salomonis sp. nov., a canine gastric Helicobacter sp. related to Helicobacter felis and Helicobacter bizzozeronii.

During a study of the prevalence and distribution of gastric helicobacters in domestic pets, a novel group of Helicobacter-like organisms were identified. These "Helicobacter group 2" strains were initially distinguished from the species Helicobacter felis and Helicobacter bizzozeronii by their cellular morphology and the type of motility exhibited. Bacterial cells were only slightly spiral, 5 to 7 microns long, and 0.8 to 1.2 microns wide and showed an unusual slow wavelike motion. Each cell had tufts of sheathed flagella at one or both ends. Phylogenetic analysis by 16S ribosomal DNA sequence comparison revealed that H. felis, H. bizzozeronii, "Gastrospirillum hominis" 2, and the new group of helicobacters formed a distinct cluster with intraspecies similarity values of more than 98%. These taxa were clearly separated from all other known Helicobacter species. Dot blot DNA-DNA hybridization studies indicated that the Helicobacter group 2 strains are genetically homogeneous and distinct from other canine and feline gastric helicobacters. Quantitative DNA-DNA hybridization experiments showed that Helicobacter group 2 strains exhibit > 90% DNA homology to each other, but < 39% homology to the phylogenetically related taxa H. felis and H. bizzozeronii. We propose the name Helicobacter salomonis for the novel Helicobacter group 2 strains. The type strain is H. salomonis Inkinen (= CCUG 37845).

Animals↗
PubMed2002

Helicobacter nemestrinae ATCC 49396T is a strain of Helicobacter pylori (Marshall et al. 1985) Goodwin et al. 1989, and Helicobacter nemestrinae Bronsdon et al. 1991 is therefore a junior heterotypic synonym of Helicobacter pylori.

Helicobacter nemestrinae Bronsdon et al. 1991, a gastric helicobacter species isolated from a pigtailed macaque, is thought to be the species most closely related to the important human pathogen Helicobacter pylori. The only available strain of this taxon is the type strain, ATCC 49396T. We sequenced seven housekeeping genes and two flagellin genes for H. nemestrinae ATCC 49396T. If ATCC 49396T were a separate species, these sequences should have been distinct from those of H. pylori. Instead, all sequences clustered together with sequences obtained previously for 20 or more H. pylori isolates from diverse geographical locations. The 16S rDNA sequence differed from that reported previously for this strain by 38 nucleotides and was most similar to that of H. pylori 85D08 (accession no. U00769), which was isolated from a rhesus macaque. It differed by less than 1% from 16S rDNA sequences of numerous other H. pylori strains, including the type strain, NCTC 11637T (= ATCC 43504T). These data indicate that the strain currently distributed as H. nemestrinae ATCC 49396T is really a strain of H. pylori and that H. nemestrinae Bronsdon et al. 1991 is a junior heterotypic synonym of Helicobacter pylori (Marshall et al. 1985) Goodwin et al. 1989.

Animals↗
PubMed2004

Intact gram-negative Helicobacter pylori, Helicobacter felis, and Helicobacter hepaticus bacteria activate innate immunity via toll-like receptor 2 but not toll-like receptor 4.

Molecular and genetic studies have demonstrated that members of the Toll-like receptor (TLR) family are critical innate immune receptors. TLRs are recognition receptors for a diverse group of microbial ligands including bacteria, fungi, and viruses. This study demonstrates that distinct TLRs are responsible for the recognition of Helicobacter lipopolysaccharide (LPS) versus intact Helicobacter bacteria. We show that the cytokine-inducing activity of Helicobacter LPS was mediated by TLR4; i.e., TLR4-deficient macrophages were unresponsive to Helicobacter pylori LPS. Surprisingly, the cytokine response to whole Helicobacter bacteria (H. pylori, H. hepaticus, and H. felis) was mediated not by TLR4 but rather by TLR2. Studies of HEK293 transfectants revealed that expression of human TLR2 was sufficient to confer responsiveness to intact Helicobacter bacteria, but TLR4 transfection was not sufficient. Our studies further suggest that cag pathogenicity island genes may modulate the TLR2 agonist activity of H. pylori as cagA+ bacteria were more active on a per-cell basis compared to cagA mutant bacteria for interleukin-8 (IL-8) cytokine secretion. Consistent with the transfection studies, analysis of knockout mice demonstrated that TLR2 was required for the cytokine response to intact Helicobacter bacteria. Macrophages from both wild-type and TLR4-deficient mice produced a robust cytokine secretion response (IL-6 and MCP-1) when stimulated with intact Helicobacter bacteria. In contrast, macrophages from TLR2-deficient mice were profoundly unresponsive to intact Helicobacter stimulation, failing to secrete cytokines even at high (100:1) bacterium-to-macrophage ratios. Our studies suggest that TLR2 may be the dominant innate immune receptor for recognition of gastrointestinal Helicobacter species.

Animals↗
PubMed2002

Immunogenic proteins of Helicobacter pullorum, Helicobacter bilis and Helicobacter hepaticus identified by two-dimensional gel electrophoresis and immunoblotting.

The ecological niches occupied by various species of Helicobacter are not yet known and the full spectrum of diseases associated with Helicobacter infections are not yet defined. Since these fastidious microaerofilic bacteria require special growth conditions new and improved molecular and serologic diagnostic methods have been developed to increase our understanding of their pathogenesis and virulence characteristics. Immunogenic cell surface proteins of Helicobacter pullorum, Helicobacter bilis, and Helicobacter hepaticus were characterised by proteomic techniques using two-dimensional electrophoresis and immunoblotting with antisera from immunised rabbits. Cross-reactivity between the three Helicobacter species were analysed after a four-step cross-absorption experiment. For H. pullorum, H. bilis and H. hepaticus 21, 13 and 27 specific immunogenic proteins, respectively, were identified. These proteins could be of important sero-diagnostic value for analyses of sera from humans, laboratory animals and for the veterinarian field.

Antigens, Bacterial↗
PubMed1995

Comparative ultrastructural and functional studies of Helicobacter pylori and Helicobacter mustelae flagellin mutants: both flagellin subunits, FlaA and FlaB, are necessary for full motility in Helicobacter species.

Helicobacter mustelae causes chronic gastritis and ulcer disease in ferrets. It is therefore considered an important animal model of human Helicobacter pylori infection. High motility even in a viscous environment is one of the common virulence determinants of Helicobacter species. Their sheathed flagella contain a complex filament that is composed of two distinctly different flagellin subunits, FlaA and FlaB, that are coexpressed in different amounts. Here, we report the cloning and sequence determination of the flaA gene of H. mustelae NCTC12032 from a PCR amplification product. The FlaA protein has a calculated molecular mass of 53 kDa and is 73% homologous to the H. pylori FlaA subunit. Isogenic flaA and flaB mutants of H. mustelae F1 were constructed by means of reverse genetics. A method was established to generate double mutants (flaA flaB) of H. mustelae F1 as well as H. pylori N6. Genotypes, motility properties, and morphologies of the H. mustelae flagellin mutants were determined and compared with those of the H. pylori flaA and flaB mutants described previously. The flagellar organizations of the two Helicobacter species proved to be highly similar. When the flaB genes were disrupted, motility decreased by 30 to 40%. flaA mutants retained weak motility by comparison with strains that were devoid of both flagellin subunits. Weakly positive motility tests of the flaA mutants correlated with the existence of short truncated flagella. In H. mustelae, lateral as well as polar flagella were present in the truncated form. flaA flaB double mutants were completely nonmotile and lacked any form of flagella. These results show that the presence of both flagellin subunits is necessary for complete motility of Helicobacter species. The importance of this flagellar organization for the ability of the bacteria to colonize the gastric mucosa and to persist in the gastric mucus remains to be proven.

Amino Acid Sequence↗
PubMed2000

Eradication of helicobacter pylori for non-ulcer dyspepsia.

BACKGROUND: Helicobacter pylori (H pylori) is the main cause of peptic ulcer disease. The role of H pylori in non-ulcer dyspepsia is less clear. OBJECTIVES: To determine the effect of H pylori eradication on dyspepsia symptoms and quality of life scores in patients with non-ulcer dyspepsia. SEARCH STRATEGY: Trials were identified through electronic searches of the Cochrane Controlled Trials Register (CCTR), MEDLINE, EMBASE, CINAHL and SIGLE, using appropriate subject headings and keywords, searching bibliographies of retrieved articles, and through contacts with experts in the fields of dyspepsia and with pharmaceutical companies. SELECTION CRITERIA: All parallel group randomised controlled trials (RCTs) comparing drugs to eradicate H pylori with placebo or other drugs known not to eradicate H pylori for patients with non-ulcer dyspepsia. DATA COLLECTION AND ANALYSIS: Data were collected on individual and global dyspeptic symptom scores, quality of life measures and adverse effects. Dyspepsia outcomes were dichotomised into minimal/resolved versus same/worse symptoms. MAIN RESULTS: Seven randomised controlled trials were included in the systematic review. Five trials compared proton pump inhibitor dual or triple therapy with a proton pump inhibitor + placebo antibiotics, and evaluated dyspepsia at 6-12 months in 1,385 patients. H pylori eradication was significantly superior to placebo in treating non ulcer dyspepsia (relative risk reduction = 7%; 95% CI = 1% to 12%; p=0.02) and there was no significant heterogeneity between the studies. The number needed to treat to cure one case of dyspepsia = 19 (95% CI = 11 to 132). A further two trials compared Bismuth based H pylori eradication with an alternative pharmacological agent. These trials were smaller and had a shorter follow-up but suggested H pylori eradication was more effective than either H2 receptor antagonists or sucralfate in treating non-ulcer dyspepsia. REVIEWER'S CONCLUSIONS: H pylori eradication may be an effective therapy for H pylori positive non-ulcer dyspepsia. This result is not robust and further evidence on the efficacy of H pylori eradication in non ulcer dyspepsia would be helpful. The effect is modest and economic models would help establish whether this approach is cost-effective. This review will be updated as results from other ongoing trials (Malfertheiner 2000) are made available.

Anti-Bacterial Agents↗
PubMed2003

Helicobacter sp. flexispira 16S rDNA taxa 1, 4 and 5 and Finnish porcine Helicobacter isolates are members of the species Helicobacter trogontum (taxon 6).

The term 'flexispira' refers to micro-organisms with a particular morphology: fusiform-shaped with helical periplasmic fibrils and bipolar tufts of sheathed flagella. Two flexispira taxa have been formally named, Helicobacter bilis and Helicobacter trogontum, a third named species is Helicobacter aurati and eight additional 16S rRNA sequence-based flexispira taxa have been described by Dewhirst et al. (Int J Syst Evol Microbiol 50, 1781-1787, 2000) and given the provisional designation Helicobacter sp. flexispira taxa 1-5, 7, 8 and 10. In the present study, seven gastric or intestinal flexispira isolates from seven Finnish pigs originating from different farms were characterized. Morphologically, all these porcine isolates had typical flexispira morphology. Analysis of the 16S rDNA sequences of five isolates showed that they were most closely related to the sequences of flexispira taxa 4 and 5 and H. trogontum (taxon 6), but less closely related to taxa 1-3 and 8, H. bilis and H. aurati. Phenotypic characterization, analysis of RFLPs of 16S and 23S rDNAs and SDS-PAGE profiles revealed that all of the porcine isolates, reference strains of flexispira taxa 1, 4 and 5 and the type strain of H. trogontum (ATCC 700114T) had highly related characteristics that differed from those of the reference strains of taxa 2, 3 and 8 and H. bilis. Furthermore, a high DNA-DNA binding rate was found, in dot-blot hybridization studies, between the Finnish porcine strains, taxa 1, 4 and 5 reference strains and H. trogontum ATCC 700114T. In conclusion, polyphasic characterization of novel porcine flexispira isolates and previously described taxa 1, 4 and 5 reference strains showed that they all belong to a validly described species, H. trogontum, and that the taxonomy of known flexispiras is less complicated than proposed on the basis of 16S rDNA sequence analysis.

Animals↗
PubMed2001

Evaluation of a group-specific 16S ribosomal DNA-based PCR for detection of Helicobacter bizzozeronii, Helicobacter felis, and Helicobacter salomonis in fresh and paraffin-embedded gastric biopsy specimens.

A new specific and sensitive 16S ribosomal DNA-based PCR assay was developed. The assay targets a 78-bp DNA fragment unique to Helicobacter bizzozeronii, Helicobacter felis, and Helicobacter salomonis and can be used with freshly frozen and formalin-fixed paraffin-embedded gastric biopsy specimens.

Animals↗
PubMedDate not supplied

The inflammatory response in the mouse stomach to Helicobacter bizzozeronii, Helicobacter salomonis and two Helicobacter felis Strains.

The inflammatory response in the mouse stomach was evaluated as a means of distinguishing different non-pylori Helicobacter (H.) strains in terms of virulence. Mice of four strains (BALB/c, SJL, C57BL/6 and CFW) were infected intragastrically with four bacterial strains (H. felis ATCC 49179 and CCUG 37471, H. bizzozeronii and H. salomonis). The animals were killed for gastric examination at 3, 9 or 16 weeks post-inoculation. H. salomonis could not be detected by the polymerase chain reaction, but the other three organisms were detected in all stomach samples at all timepoints. SJL mice consistently showed particularly severe gastric inflammation regardless of bacterial strain. Lymphocytes and occasionally neutrophils were seen in submucosa and lamina propria mucosae. BALB/c mice showed the least severe inflammatory changes. H. bizzozeronii differed from the two H. felis strains in producing less striking pathological changes in mice. Of the two H. felis strains, ATCC 49179 produced the more severe inflammatory changes in SJL mice.

Animals↗
PubMed1999

Differential features of gastric cancer patients, either Helicobacter pylori positive or Helicobacter pylori negative.

BACKGROUND: Helicobacter pylori infection is associated with an increased risk of gastric cancer. In Helicobacter pylori negative patients, factors different from those in Helicobacter pylori positive patients may be involved in gastric carcinogenesis. METHODS: Thirty-nine recently diagnosed consecutive patients with gastric cancer were investigated. Gastric biopsies were obtained for detection of Helicobacter pylori (by immunohistochemistry), non-Helicobacter pylori flora (by modified Giemsa and culture) and histological assessment according to the Sydney classification by Haematoxylin-Eosin staining. In serum samples, Helicobacter pylori antibodies were determined by IgG enzyme-linked immunosorbent assay, IgA enzyme-linked immunosorbent assay, and Western blotting. Furthermore, serum gastrin, pepsinogen A and C and plasma chromogranin A were determined. RESULTS: Helicobacter pylori was detected by immunohistochemistry in 53.8%, by IgG in 56.4%, by IgA in 33.3%, and by Western blotting in 74.4% of the 39 patients. Ten patients (25.6%) were negative by both histology and serology. Non-Helicobacter pylori flora was detected in 27 of the 39 patients (69.2%) with a similar frequency in Helicobacter pylori positive and negative patients. Helicobacter pylori positivity was found significantly more often in diffuse than intestinal type carcinoma patients (p < 0.05). Elevated gastrin levels and antrum-sparing atrophic gastritis were more frequent in Helicobacter pylori negative than in Helicobacter pylori positive patients (p < 0.05). CONCLUSIONS: In 10 out of 39 gastric cancer patients, no evidence of previous or current Helicobacter pylori infection could be demonstrated. Non-Helicobacter pylori was found in 69.2% of patients regardless of the Helicobacter pylori status. Further studies are needed to establish the contribution of non-Helicobacter pylori flora as well as antrum-sparing atrophic gastritis with hypergastrinaemia to the development of gastric cancer.

Aged↗
PubMed2003

Assessment of PCR-DGGE for the identification of diverse Helicobacter species, and application to faecal samples from zoo animals to determine Helicobacter prevalence.

Helicobacter species are fastidious bacterial pathogens that are difficult to culture by standard methods. A PCR-denaturing gradient gel electrophoresis (PCR-DGGE) technique for detection and identification of different Helicobacter species was developed and evaluated. The method involves PCR detection of Helicobacter DNA by genus-specific primers that target 16S rDNA and subsequent differentiation of Helicobacter PCR products by use of DGGE. Strains are identified by comparing mobilities of unknown samples to those determined for reference strains; sequence analysis can also be performed on purified amplicons. Sixteen DGGE profiles were derived from 44 type and reference strains of 20 Helicobacter species, indicating the potential of this approach for resolving infection of a single host by multiple Helicobacter species. Some more highly related species were not differentiated whereas in highly heterogeneous species, sequence divergence was observed and more than one PCR-DGGE profile was obtained. Application of the PCR-DGGE method to DNA extracted from faeces of zoo animals revealed the presence of Helicobacter DNA in 13 of 16 samples; a correlation was seen between the mobility of PCR products in DGGE analysis and DNA sequencing. In combination, this indicated that zoo animals are colonized by a wide range of different Helicobacter species; seven animals appeared to be colonized by multiple Helicobacter species. By this approach, presumptive identifications were made of Helicobacter bilis and Helicobacter hepaticus in a Nile crocodile, Helicobacter cinaedi in a baboon and a red panda, and Helicobacter felis in a wolf and a Taiwan beauty snake. All of these PCR products ( approximately 400 bp) showed 100 % sequence similarity to 16S rDNA sequences of the mentioned species. These results demonstrate the potential of PCR-DGGE-based analysis for identification of Helicobacter species in complex ecosystems, such as the gastrointestinal tract, and could contribute to a better understanding of the ecology of helicobacters and other pathogens with a complex aetiology.

Animals↗
PubMed1999

Colonization and tissue tropism of Helicobacter pylori and a novel urease-negative Helicobacter species in ICR mice are independent of route of exposure.

BACKGROUND: In humans, Helicobacter pylori is known to colonize the stomach and to induce persistent gastritis; selected reports also suggest it causes extragastric disease, including hepatitis. H. pylori and a novel urease-negative Helicobacter sp. induce gastritis and typhlocolitis, respectively, when inoculated orally into mice. Experimental typhlocolitis and hepatitis have been caused by intraperitoneal (i.p.) injection of H. hepaticus, H. bilis, and the novel Helicobacter spp. However, the route by which i.p.-inoculated organisms localize to specific areas of the gastrointestinal system is unknown. MATERIALS AND METHODS: To determine whether Helicobacter spp. can be isolated from blood, can preferentially colonize specific tissues, and can cause pathological changes, we inoculated 6-week-old outbred mice orally or intraperitoneally with H. pylori or a novel Helicobacter sp. RESULTS: When these mice were inoculated by the i.p. route, H. pylori was cultured from lungs, spleen, liver, cecum, and stomach on day 1 after inoculation, from liver and stomach mucosa on day 3 after inoculation, and from the stomach on day 30 after inoculation, suggesting preferential colonization of the stomach. After inoculation by the i.p. route, the novel intestinal Helicobacter sp. was cultured from the blood, lungs, spleen, liver, kidneys, cecum, and feces but not from stomach mucosa on day 1 after inoculation. By day 30 after inoculation, the novel Helicobacter sp. was cultured from cecum and feces only, suggesting that it had preferentially colonized the lower bowel. By the i.p. route, the novel Helicobacter sp. induced hepatitis that persisted for 30 days after inoculation. Though mice inoculated intraperitoneally with H. pylori developed an acute hepatitis, the liver lesion began to resolve 30 days after inoculation. Mice inoculated orally with either H. pylori or the novel Helicobacter sp. did not have hepatitis on day 30 after inoculation but developed 100% colonization of stomach and cecum, respectively. CONCLUSION: The isolation of H. pylori and the novel Helicobacter sp. from multiple tissues infers that a transient helicobacter bacteremia occurs when Helicobacter spp. are injected intraperitoneally, but organisms are cleared rapidly from nontarget tissues and preferentially colonize specific regions of the gastrointestinal tract.

Animals↗
PubMed2000

Identification of Helicobacter pylori and other Helicobacter species by PCR, hybridization, and partial DNA sequencing in human liver samples from patients with primary sclerosing cholangitis or primary biliary cirrhosis.

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, and Helicobacter hepaticus. Samples from patients with primary biliary cirrhosis and primary sclerosing cholangitis (11 and 9 samples, respectively) were positive by PCR with Helicobacter genus-specific primers. Of these 20 samples, 8 were positive with the 16S rRNA primer and 9 were positive with the 26-kDa protein primer of H. 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 the Helicobacter 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. Helicobacter positivity 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.

Alkaline Phosphatase↗
PubMed2005

Detection of non-pylori Helicobacter species in "Helicobacter heilmannii"-infected humans.

BACKGROUND: A small proportion of patients suffering from chronic active gastritis are diagnosed with gastric Helicobacter species other than Helicobacter pylori. Circumstantial evidence has suggested that these bacteria, also referred to as "Helicobacter heilmannii"-like organisms (HHLO), may be transmitted through animals. The isolation of a Helicobacter bizzozeronii strain from a human patient confirmed this hypothesis. It was the aim of the present study to assess the presence of animal Helicobacter species and H. pylori in humans infected with HHLO, as diagnosed by histology. METHODS: Paraffin-embedded gastric biopsy specimens of 108 HHLO-infected patients (42 women and 66 men) from three clinical centers were screened for the presence of animal gastric Helicobacter species by polymerase chain reaction (PCR), using assays targeting the 16S rDNA region of the three known canine and feline helicobacters (H. bizzozeronii, H. salomonis and H. felis), "Candidatus H. suis", and "Candidatus H. bovis". In addition, the presence of H. pylori was evaluated by multiplex PCR analysis. RESULTS: In 63.4% of the stomachs (64/101) classification of the Helicobacter infection into the above mentioned groups was achieved. Non-pylori Helicobacter species commonly colonizing the stomachs of cats and dogs were found in 48.5% (49/101) of the patients. Fourteen (13.9%) samples tested positive for "Candidatus H. suis", and "Candidatus H. bovis" was demonstrated in 1 (0.9%) patient. The presence of H. pylori was established in 13 patients (12.9%). Eleven stomachs (10.9%) were infected with at least two different Helicobacter species. CONCLUSIONS: This study identifies animal Helicobacter species in the stomach of a large series of HHLO-infected patients, which may have clinical implications in a subset of patients with gastric disease.

Adolescent↗
PubMed2004

Diagnosis of Helicobacter pylori infection and diseases associated with Helicobacter pylori by Helicobacter pylori outer membrane proteins.

AIM: To examine the serological response of patients with upper gastrointestinal diseases and Helicobocter pylori (H pylori) infection to two H pylori outer membrane proteins (OMPs) (Mr18,000 and Mr 26,000) acquired by gene recombinant technique, and to determine the diagnostic significance of serological tests derived from these OMPs. METHODS: Recombinant vectors encoding the two H pylori OMPs were used to transform and express in BL21 (DE3) E.coli. After purification with Ni2+-NTA agarose resin, colloid gold kits were prepared with purified recombinant proteins to detect H pylori infection and H pylori-associated diseases by the immunity-marker technology. We selected 150 patients with H pylori infection and digestive symptoms without previous treatment, including chronic gastritis (n = 60), duodenal ulcer (n = 30), gastric ulcer (n = 30), and gastric cancer (n = 30). As controls, 33 H pylori-negative healthy volunteers were also recruited. Serum samples were collected from all subjects, and the antibodies to specific proteins of H pylori were tested with the colloid gold test kits. The sensitivity, specificity and accuracy of the colloid gold tests were evaluated, by using the combination of standard diagnostic methods (13C urea breath test and bacteria culture) and classic enzyme-linked immunosorbent assay (ELISA) as reference. RESULTS: After purification with Ni2+-NTA agarose resin, the purity of recombinant fusion proteins was about 95%. The recombinant fusion proteins were recognized by the specific monoclonal antibodies against the two H pylori OMPs, as demonstrated by the ELISA. Of the 150 serum samples from patients infected with H pylori 141 (94.0%) responded positively to the recombinant protein with Mr 26,000, while the seropositive rates were 95.0%, 96.7%, 96.7% and 90.0% for patients with H pylori-associated chronic gastritis, duodenal ulcer, gastric ulcer, and gastric cancer respectively. The sensitivity, specificity, and accuracy of the colloid gold kit with Mr 26,000 protein were 94.0%, 97.0%, and 94.5%, respectively. Compared with the classic ELISA, bacteria culture and 13C urea breath test results in detecting H pylori-infection, there was no significant difference (P>0.05). For the colloid gold kit with Mr 18,000, the seropositive rates were 52.0%, 40.0%, 40.0%, 53.3% and 86.7%, respectively, in H pylori-infected patients, and those with H pylori-associated chronic gastritis, duodenal ulcer, gastric ulcer, and gastric cancer. There was a significant difference (P<0.05) in seropositivity between patient with gastric cancer (86.7%) and those with other diseases (43.3%). CONCLUSION: The two colloid gold kits derived from the recombinant OMPs are useful tools either for detecting H pylori infection, or for, predicting H pylori-associated gastric malignancy.

Adult↗
PubMed2001

Helicobacter spp. infection in cats: evaluation of the humoral immune response and prevalence of gastric Helicobacter spp.

The principal aims of this study were to evaluate the humoral immune response (IgG) of cats with gastric Helicobacter spp. infection, and to determine the prevalence of different types of Helicobacter spp. in the stomachs of cats. The Helicobacter infection status of 45 cats (12 healthy spay/neuter cats, 9 sick cats, 24 colony cats) was determined by evaluating endoscopic gastric biopsies for urease activity, presence of Helicobacter-like organisms (HLO) on histopathology, and genus and species-specific PCR. Serum samples were evaluated with a kinetic enzyme linked immunosorbent assay (ELISA) utilizing the high molecular cell-associated protein (HM-CAP) fraction of H. felis ATCC 49179.Seventeen of 45 cats were infected with Helicobacter spp.: "H. heilmannii" 9/17, H. felis 4/17, mixed "H. heilmannii" and H. felis 3/17, unclassified-Helicobacter spp. 7/17. H. pylori was not detected in any cat. Kinetic ELISA results were significantly higher for infected cats, than for uninfected cats. Cats infected with different Helicobacter spp. showed similar distribution of OD/min values. There were no effects of age or clinical signs on the results of kinetic ELISA. No correlation between colonization density and seroconversion was observed. There were statistically significant, but weak correlations between the degree of seroconversion and the degree of inflammation, and the number of lymphoid follicles. Infected cats had more severe inflammation in the pylorus and fundus than uninfected cats. Infected sick cats had a higher degree of pyloric, but not fundic inflammation, than healthy infected cats and uninfected sick cats. The results indicate that naturally acquired infection with gastric Helicobacter spp. is associated with seroconversion (IgG) in cats. The similar ELISA values in cats infected with a variety of Helicobacter spp. suggests substantial antigenic homology between different Helicobacter spp. The higher degree of inflammation in infected than uninfected cats, supports a role for Helicobacter as a cause of gastritis in cats.

Animals↗
PubMed2003

Depletion of neutrophils in IL-10(-/-) mice delays clearance of gastric Helicobacter infection and decreases the Th1 immune response to Helicobacter.

Gastric infection with Helicobacter induces a lymphocyte-rich mucosal inflammation that contains a minor population of neutrophilic granulocytes. The function of neutrophils in the local immune response to gastric Helicobacter infection remains unknown. To investigate this issue, we conducted experiments in neutrophil-depleted control wild-type (wt) and IL-10(-/-) mice infected with Helicobacter felis by gastric lavage. Infection of wt mice elicited a mild, focal gastritis and a Helicobacter-specific Th1 immune response. In wt mice Helicobacter colonization of the stomach was persistent and progressively increased during the 29 days of observation. Infection of IL-10(-/-) mice with H. felis elicited a severe chronic gastritis and a greatly enhanced Helicobacter-specific Th1 immune response, as compared with wt mice. After initial colonization, the IL-0(-/-) mice completely cleared Helicobacter from the stomach by day 8. The gastric inflammation in wt and IL-10(-/-) mice contained modest numbers of neutrophils. The intensity of gastric inflammation and the extent of Helicobacter colonization were similar in control and in neutrophil-depleted wt mice. In contrast, neutrophil depletion of Helicobacter-infected IL-10(-/-) mice decreased the severity of gastritis, modulated the Helicobacter-specific Th1 immune response, and delayed the clearance of bacteria from the stomach. These studies identify a role for neutrophils in the local and systemic immune response to gastric Helicobacter in IL-10(-/-) mice.

Animals↗
PubMedDate not supplied

A 3-day anti-Helicobacter pylori therapy is a good alternative for bleeding peptic ulcer patients with Helicobacter pylori infection.

BACKGROUND/AIMS: One-week triple therapy has been recommended as a standard regimen for eradicating Helicobacter pylori infection. The emergence of antibiotic-resistant strains, adverse drug effects, poor compliance and high cost of therapy add problems to the management of these patients. In this study, we assessed whether a 3-day triple therapy could be effective in eradicating Helicobacter pylori infection in bleeding peptic ulcer patients. METHODOLOGY: Peptic ulcer patients with Helicobacter pylori infection were enrolled in this study. Patients enrolled at the outpatient department (group A) received a 7-day oral regimen: bismuth subcitrate colloid 300 mg + amoxicillin 500 mg + metronidazole 250 mg four times per day. Patients who were admitted to the wards due to peptic ulcer bleeding (group B) received a 3-day regimen including omeprazole 40 mg intravenously every 6 hours, amoxicillin 500 mg + metronidazole 250 mg orally four times daily after hemostasis had been achieved. Patients of both groups received omeprazole 20 mg once per day or cimetidine 400 mg twice daily per os for at least-one month after anti-Helicobacter pylori therapy. We followed every patient endoscopically two months after anti-Helicobacter pylori therapy. RESULTS: From June 1997 to April 1999, a total of 57 patients (30 in group A and 27 in group B) with gastric or duodenal ulcer and Helicobacter pylori infection completed anti-Helicobacter pylori therapy. Two months after anti-Helicobacter pylori therapy, peptic ulcer was found to be healed with a scar in 26 (86.7%) of group A and 23 (85.2%) of group B (P > 0.1). The eradication rates of Helicobacter pylori in the two groups were not significantly different in an intention-to-treat analysis [group A: 78.8% (26/33), 95% CI: 64.9-92.7%; group B: 80% (24/30), 95% CI: 65.7-94.3%, P > 0.1] and in a per protocol analysis [group A: 86.7% (26/30), 95% CI: 74.5-98.9%, group B: 88.9% (24/27), 95% CI: 77.1-100.7%, P > 0.1]. Fewer side effects occurred in group B (3/30) than those in group A (7/33) (P > 0.1). CONCLUSIONS: In patients with peptic ulcer bleeding a 3-day anti-Helicobacter pylori therapy is a good alternative for eradicating Helicobacter pylori infection.

Adult↗