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PubMed1998

[Colonic microenvironment in familial helicobacter infection].

To elucidate the significance of the familial microenvironment in the genesis of Helicobacter infection, a clinical and instrumental investigation was made of 13 families selected by the probands who had digestive diseases associated with H. pylori: gastroduodenitis and duodenal ulcer disease. The occurrence of Helicobacter infection and gastritis in the family members was ascertained to be largely determined by their concurrent residence in the limited area, i.e. by the way of life. The contribution of the "family" factor in antral gastritis, fundal gastritis, and H. pylori infection was 60.0, 40.0, and about 90.0%, respectively. The patients with gastroenterological abnormalities associated with H. pylori were found to show changes in the species-specific and quantitative composition of the colonic microbiocenosis, which were symptomatic and revealed by bacteriological studies in 47.5% of cases and severe in 32.5%. When antihelicobacter therapy is planned, a through treatment of all family members and, if possible, pets should be made. Colonic microbiocenosis should be monitored while treating Helicobacter infection.

Adolescent↗

PubMed1999

Gastric Helicobacter infection in dogs.

Infection with gastric Helicobacter spp. is prevalent in dogs and is not accompanied by clinical signs in the majority of cases. Five different Helicobacter spp. have been found in the canine stomach. The modes of transmission are unclear, but fecal-oral, oral-oral, and surface water transmission are all possible. A diagnosis can be made using invasive or biopsy-based tests, but noninvasive techniques using UBBT and serology hold promise for the future.

Animals↗

PubMed2005

[Association between Helicobacter infection in liver tissue and primary liver carcinoma].

OBJECTIVE: To investigate the relationship between Helicobacter species and primary liver carcinoma (PLC). METHODS: The liver samples resected during operation from 21 patients with PLC diagnosed by histopathology and 12 patients with other liver diseases as controls were studied. Helicobacter species in liver specimens from the studied subjects were examined by PCR with Helicobacter specific 16SrRNA primers. The amplified products were identified by Southern hybridization and nucleic acid hybridization in situ and sequencing. The specimens were made slices to undergo in situ hybridization of cDNA-mRNA of Helicobacter. Qualitative and quantitative studies were used to assess the correlation of liver tissue helicobacter infection with PLC. RESULTS: Thirteen of the 21 samples (62%) of PLC were positive for Helicobacter specific 16SrRNA gene, while none was positive in the controls (P < 0.01). In situ hybridization results demonstrated a highly Helicobacter 16SrRNA-mRNA positive rate in the PLC group (62%) and none of positive specimen in the control group (P < 0.01). Nine of the Helicobacter specific PCR applicants were sequenced and a homology of 97.80% in comparison with 16SrRNA of H p was found. CONCLUSION: Helicobacter infection may exist in the liver tissues of PLC patients with a high infection rate, suggesting an association between Helicobacter infection and PLC.

Adult↗

PubMed1995

Oral immunization with Helicobacter pylori urease B subunit as a treatment against Helicobacter infection in mice.

BACKGROUND & AIMS: Eradication of Helicobacter pylori infections in humans results in the healing of gastritis and gastric ulcers. This study used a mouse model to test whether oral vaccination can cure Helicobacter infection and gastritis. METHODS: Mice were infected with Helicobacter felis. Three weeks after infection, the mice were orally immunized with H. pylori urease B subunit. Control mice were simultaneously infected but sham immunized. RESULTS: Three to 8 weeks after oral immunization of H. felis-infected mice with recombinant H. pylori urease B subunit, the infection cleared and there was no evidence of gastritis. Vaccinated mice remained protected against two consecutive H. felis challenges. CONCLUSIONS: These results show that the lack of natural immunity against Helicobacter can be overcome by oral immunization and that vaccination offers a novel therapeutic approach to Helicobacter-induced gastritis.

Administration, Oral↗

PubMed1996

A quantitative analysis of symptoms of non-ulcer dyspepsia as related to age, pathology, and Helicobacter infection.

BACKGROUND: Non-ulcer dyspepsia (NUD) has been attributed to gastritis and Helicobacter infection. The Sydney classification enables dyspepsia symptoms to be assessed quantitatively in relation to Helicobacter infection and topographic pathology in different gastric compartments. METHODS: In this study of 348 patients with NUD we studied the unconfounded effects of age, pathology, and Helicobacter. Endoscopic findings, dyspeptic symptoms, and age were recorded prospectively. Multiple logistic regression was used to evaluate the independent effects of age, pathology, and Helicobacter. RESULTS: Ulcer-like pain was negatively related to age (odds ratio = 0.75/10 years; P < 0.001). A high density of Helicobacter at the antrum but not elsewhere in the stomach was positively related to ulcer-like pain (odds ratio = 3.38; P < 0.002). Adjusted for age, none of the endoscopic (P > 0.19) and histopathology findings (P > 0.09) played an important role in NUD. CONCLUSION: Age was the most important determinant of dyspeptic symptoms, but not pathology or Helicobacter.

Abdominal Pain↗

PubMed1994

Helicobacter infection and gastric ethanol metabolism.

The organism frequently colonizing the stomach of patients suffering from chronic active gastritis and peptic ulcer disease--Helicobacter pylori--possesses marked alcohol dehydrogenase (ADH) activity. Consequently, Helicobacter infection may contribute to the capacity of the stomach to metabolize ethanol and lead to increased acetaldehyde production. To study this hypothesis, we first determined ADH activity in a variety of H. pylori strains originally isolated from human gastric mucosal biopsies. ADH activity was also measured in endoscopic gastric mucosal specimens obtained from H. pylori-positive and -negative patients. Furthermore, we used a mouse model of Helicobacter infection to determine whether infected animals exhibit more gastric ethanol metabolism than noninfected controls. Most of the 32 H. pylori strains studied possessed clear ADH activity and produced acetaldehyde. In humans, gastric ADH activity of corpus mucosa did not differ between H. pylori-positive and -negative subjects, whereas in antral biopsies ADH activity was significantly lower in infected patients. In mice, gastric ADH activity was similar or even lower in infected animals than in controls, depending on the duration of infection, despite the fact that the infectious agent used--Helicobacter felis--showed ADH activity in vitro. In accordance with this, Helicobacter infection tended to decrease rather than increase gastric ethanol metabolism in mice. In humans, it remains to be established whether the observed decrease in antral ADH activity associated with H. pylori infection can lead to reduced gastric first-pass metabolism of ethanol.

Acetaldehyde↗

PubMed2006

Helicobacter infection in hepatocellular carcinoma tissue.

AIM: To investigate whether Helicobacter species (Helicobacter spp.) could be detected in hepatocellular carcinoma (HCC) tissue. METHODS: Liver samples from 28 patients with hepatocellular carcinoma (HCC) diagnosed by histopathology were studied. Twenty-two patients with other liver diseases (5 with liver trauma, 7 with cavernous liver hemangioma, 6 with liver cyst and 4 with hepatolithiasis), 25 patients with gastric cancer, 15 with colonic cancer and 15 with myoma of uterus served as controls. Two pieces of biopsy were obtained from each patient. One was cultured for Helicobacter spp. and extraction of DNA, the other was prepared for scanning electron microscopy (SEM) and in situ hybridization. The samples were cultured on Columbia agar plates with microaerobic techniques. Helicobacter spp. in biopsy from the studied subjects was detected by polymerase chain reaction (PCR) with Helicobacter spp. 16S rRNA primers. Amplified products were identified by Southern hybridization and sequenced further. Besides, other genes (vacA, cagA) specific for Helicobacter pylori (H pylori) were also detected by PCR. Helicobacter spp. in biopsies was observed by SEM. Transmission electron microscopy (TEM) was performed to identify the cultured positive Helicobacter spp. The presence of Helicobacter spp. was detected by in situ hybridization to confirm the type of Helicobacter. RESULTS: The positive rate of Helicobacter cultured in HCC and gastric cancer tissue was 10.7% (3/28) and 24% (6/25), respectively. Helicobacter microorganisms were identified further by typical appearance on Gram staining, positive urease test and characteristic colony morphology on TEM. The bacterium was observed in adjacent hepatocytes of the two HCC samples by SEM. The number of cocci was greater than that of bacilli. The bacterium was also found in four gastric cancer samples. PCR showed that the positive rate of HCC and gastric cancer samples was 60.7% and 72% respectively, while the controls were negative (P<0.01). The PCR-amplified products were identified by Southern hybridization and sequenced. The homology to 16S rRNA of H pylori was 97.80%. The samples were verified by in situ hybridization for Helicobacter spp. 16S rRNA-mRNA and proved to be H pylori positive. There was no statistical significance between HCC and gastric cancer (P>0.05), but the positive rate of HCC and controls had statistical significance (P<0.01). Only 3 HCC samples and 2 gastric cancer samples of the cagA genes were detected. None of the samples reacted with primers for vacA in the two groups. As for the genotype of H pylori, type II had preference over type I. CONCLUSION: Helicobacter infection exists in liver tissues of HCC patients. Helicobacter spp. infection is related with HCC, which needs further research.

Base Sequence↗

PubMed1995

Helicobacter infections in laboratory animals: a model for gastric neoplasias?

Evidence is rapidly accumulating that Helicobacter pylori is a major risk factor for human gastric adenocarcinomas and all low-grade B-cell gastric lymphomas. Given this, there is a need to develop animal models with a view to discovering not only how carcinogenesis is initiated, but also how the process can be prevented. The lack of H. pylori animal models suitable for long-term studies means that alternatives are needed. The most productive models are likely to be the Helicobacter mustelae-infected ferret or the mouse infected with either Helicobacter felis or 'Helicobacter heilmannii'. The first evidence that helicobacter infection induces a chronic inflammation that progresses to gastric atrophy, the precursor lesion to gastric adenocarcinoma in humans, has come from the mouse model. The severity of inflammation is dependent on the type of mouse strain used, highlighting the importance of host factors in the development of gastritis. Carcinogenesis studies should only be done with mouse strains known to cause atrophy. The H. mustaelae-infected ferret appears very susceptible to the development of adenocarcinoma following ingestion of chemical carcinogens. Long-term infection of mice with H. felis results in the development of low-grade B-cell gastric lymphomas indistinguishable to those found in H. pylori-infected humans. Helicobacter-infected animals, rodents in particular are going to provide exciting opportunities to investigate not only important aspects of gastric cancer and lymphoma but also fundamental issues of carcinogenesis in general.

Animals↗

PubMed2005

Differential detection of five mouse-infecting helicobacter species by multiplex PCR.

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.

Animals↗

PubMedDate not supplied

Clinical onset of the Crohn's disease after eradication therapy of Helicobacter pylori infection. Does Helicobacter pylori infection interact with natural history of inflammatory bowel diseases?

BACKGROUND: There are conflicting reports concerning the prevalence of Helicobacter pylori infection in patients with inflammatory bowel diseases: some studies connected Sulphasalazine therapy and lower incidence of Helicobacter pylori infection, but others showed lower prevalence of Helicobacter pylori infection in inflammatory bowel diseases despite the choice of therapy. CASE REPORT: A 28-year-old male patient presented in January 1996 with the symptoms of ulcer like dyspepsia. There was no significant abnormality on physical examination, laboratory testing and abdominal ultrasound. Histology examination of the biopsy specimen taken during the upper endoscopy revealed Helicobacter pylori associated active gastritis only in the corporal part of the stomach. After two weeks eradication therapy (Omeprazole, Amoxicillin) he was well. Three months later, at the control endoscopy, granulomatous gastritis of the corporal localization was detected, without Helicobacter pylori present. Antral mucosa appeared normal, both, on endoscopy and histology examination. In July 1996 he started with cramping abdominal pain, mild periodical fever and episodes of watery diarrhea. In laboratory results we found nonspecific signs of inflammation. We repeated upper endoscopy, colonoscopy and enteroclysis--with evidence of segmental stenotic lesions of the upper part of ileum and jejunum. Again, we confirmed granulomatous gastritis and small granuloma in the proximal jejunum. After starting the 5-ASA therapy in combination with Metronidazol, patient was better clinical condition, and laboratory results were normal. We suggested mesalamine maintenance therapy 1 gr. every day, and three years later he is well, in clinical remission of Crohn's disease. CONCLUSION: The clinical course of the Crohn's disease maybe "sui generis" connected with Helicobacter pylori infection- but the exact mechanisms remain to be discovered.

Abdominal Pain↗

PubMed2005

Study on the role of gastric Helicobacter infection in gross pathological and histological lesions of the stomach in finishing pigs.

The prevalence of gastric Helicobacter infection in finishing pigs and the influence of this infection on gastric lesions was studied. Stomachs of 89 finishing pigs from 27 randomly selected herds were sampled at the slaughterhouse. Forty cases (Group A) were selected based upon the presence of gross pathological lesions in the pars oesophagea, and further 49 cases were obtained at random (Group B). Three samples of gastric tissue (junction of pars oesophagea and pars cardiaca, fundic area, and pyloric area) were collected from each stomach for histological and immunohistochemical examination. Helicobacter antigen was detected in 76 cases (85.4%). No association was found between the presence of Helicobacter in the stomach and the occurrence of gross pathological lesions in the pars oesophagea or gastritis detected on histological examination. However, a significant association was found between the occurrence of Helicobacter in the pyloric area and the presence of erosions/ulcers in the pars oesophagea (OR: 7.01, p = 0.022) in Group B. A significant association was also evident between the presence of Helicobacter and glandular lesions (dilatation of the glands + glandular abscess + degeneration of glandular epithelial cells). In conclusion, Helicobacter infection seems to be a contributing factor to pathological changes in the stomach of finishing pigs.

Animals↗

PubMed2000

Synergistic interaction between hypergastrinemia and Helicobacter infection in a mouse model of gastric cancer.

BACKGROUND & AIMS: Hypergastrinemia occurs frequently in association with acid suppression and Helicobacter infection, but its role in the progression to gastric atrophy and gastric cancer has not been well defined. METHODS: The effects of hypergastrinemia, and possible synergy with Helicobacter felis infection, were investigated in insulin-gastrin (INS-GAS) transgenic mice. RESULTS: INS-GAS mice initially showed mild hypergastrinemia, increased maximal gastric acid secretion, and increased parietal cell number but later progressed to decreased parietal cell number and hypochlorhydria. Development of gastric atrophy was associated with increased expression of growth factors, heparin-binding epidermal growth factor and transforming growth factor alpha. At 20 months of age, INS-GAS mice showed no evidence of increased enterochromaffin-like cell number, but instead exhibited gastric metaplasia, dysplasia, carcinoma in situ, and gastric cancer with vascular invasion. Invasive gastric carcinoma was observed in 6 of 8 INS-GAS mice that were >20 months old. Helicobacter felis infection of INS-GAS mice led to accelerated (< or = 8 mo) development of intramucosal carcinoma (85%), with submucosal invasion (54%) and intravascular invasion (46%; P < or = 0.05). CONCLUSIONS: These findings support the unexpected conclusion that chronic hypergastrinemia in mice can synergize with Helicobacter infection and contribute to eventual parietal cell loss and progression to gastric cancer.

Animals↗

PubMed2002

[Extra-gastrointestinal tract diseases and Helicobacter pylori infection].

Helicobacter pylori infection is linked to conditions of the upper gastrointestinal tract, including peptic ulcer and gastric adenocarcinoma na MALT lymphoma. It has also been associated with wide variety of extragastric and non-gastrointestinal conditions. However, the evidence in support of Helicobacter pylori infection as a cause of the non-gastrointestinal tract diseases is not widely understood. We reviewed the medical literature in regard to putative association of Helicobacter pylori infection and non-gastrointestinal tract condition, notably cardiovascular, autoimmune and dermatological diseases. The majority of published papers examining the potential causal relationship were case-control studies, cross-sectional and cohort studies while only a few recent articles that did not confirm the evidence of causal relationship represent well designed population-based prospective studies. The lack of clear evidence for etiopathogenetic associations of Helicobacter pylori infection and non-gastrointestinal tract conditions should focus our attention on appropriate testing and treatment of Helicobacter pylori infection in patients with conditions that are of proven association such as peptic ulcer disease.

Autoimmune Diseases↗

PubMed2005

Gastric helicobacter infection induces a Th2 phenotype but does not elevate serum cholesterol in mice lacking inducible nitric oxide synthase.

Persistent Helicobacter felis infection in (C57BL/6 x 129SvEv)F1 mice induces chronic gastritis. Expression of inducible nitric oxide synthase (iNOS) is upregulated in response to Helicobacter infection. In this study, 20 10-week-old iNOS-/- mice and 20 wild-type [(C57BL/6 x 129SvEv)F1] mice were infected with H. felis by oral gavage and were assessed histologically and serologically at 32 weeks postinfection. Equal numbers of uninfected controls were sham inoculated. The mice were scored for severity of gastric inflammation, hyperplasia, glandular atrophy, and mucous metaplasia in the corpus and for the level of helicobacter colonization. The immunoglobulin G1 (IgG1), IgG2a, and IgG2c antibody responses to H. felis were determined. As a secondary measure, serum cholesterol levels were assessed. iNOS-/- mice have a propensity for increased serum cholesterol, and although controversial, several human epidemiologic studies have demonstrated an association between Helicobacter infection and several risk factors for cardiovascular disease, including elevated serum cholesterol. Nevertheless, no differences in serum cholesterol levels were observed between the H. felis-infected and -uninfected iNOS-/- mice in this study. The uninfected animals had minimal to no gastric pathology. The gastric pathology scores for the infected animals were reduced significantly in the iNOS-deficient mice relative to those for the wild-type mice (all P <0.01). Helicobacter-infected iNOS-/- mice had chronic lymphoid infiltration and negligible to mild glandular atrophy and mucous metaplasia in the fundic mucosa, while H. felis-infected wild-type mice had severe atrophic and metaplastic mucosal changes. The atrophic gastritis in the infected wild-type mice, particularly the female mice, was also accompanied by greater granulocytic infiltration, antral hyperplasia, and diminished antral colonization, unlike that in the infected iNOS-/- mice. iNOS-/- mice developed significantly lower Th1-associated IgG2c antibody responses to H. felis (P <0.0003); the Th2-associated IgG1 responses were similar (P=0.09), suggesting a greater effect of the iNOS defect on Th1 responses. H. felis colonization was significantly greater in the iNOS-deficient mice. These findings are indicative of an impaired Th1 component of the H. felis-induced inflammatory response when the influence of iNOS is removed.

Animals↗

PubMed1998

Non-pylori Helicobacter infections in humans.

The spectrum of human non-pylori Helicobacter infections is expanding. Evidence for the presence of bacteria such as H. heilmannii, H. felis, H. rappini, H. cinaedi, H. fennelliae and H. pullorum has been reported. These bacteria are likely to be associated with different clinical disorders. H. heilmannii is the most commonly described non-pylori Helicobacter in humans. Colonization with this bacterium is usually associated with mild gastritis. In some cases, gastric ulcer disease may occur. H. heilmannii are classified as such on the basis of morphological criteria. Recent phenotypical and genotypical data suggest that this is insufficient. Therefore, for a better understanding of the relation between non-pylori Helicobacter species and disease, there is a need for studies focusing on genetic instead of morphological criteria.

Animals↗

PubMed1998

Clostridium difficile colitis associated with treatment of Helicobacter pylori infection.

Helicobacter pylori infection of the stomach is being detected and treated more often now than ever before. This is likely to result in an increase in complications such as antibiotic-associated diarrhea. However, there is no literature on the incidence of such diarrhea, particularly Clostridium difficile colitis, in patients treated for Helicobacter pylori infection. We report the case of a patient who developed Clostridium difficile colitis after treatment for Helicobacter pylori infection with metronidazole, amoxicillin, H2 blockers, and bismuth subsalicylate. This patient presented with severe diarrhea that responded to a course of metronidazole with rapid disappearance of symptoms. The incidence of Clostridium difficile colitis in patients treated for Helicobacter pylori infection has not been studied. This unique association, although not unexpected, has not yet been reported in the literature. The increasing number of patients being diagnosed and treated for this infection requires a heightened awareness on the part of physicians, to assure early diagnosis and treatment of this treatable, yet potentially dangerous, complication.

Aged↗

PubMed2002

[Gastric ulcer and Helicobacter pylori infection].

Helicobacter pylori infection and the use of non-steroidal anti-inflammatory drugs (NSAID) are considered to be the two major risk factors implicated in the development of gastric ulcer. Helicobacter pylori infection related chronic gastritis is known to be the underlying condition which may lead to gastric ulcer. Development of gastric ulcer as the consequence of underlying chronic gastritis is caused by many factors. Treating Helicobacter pylori infection entails the healing of gastric ulcer, it concomitantly prevents recurrences and complications of gastric ulcer, primarily bleeding, and changes the natural course of gastric ulcer disease. Continuation of antisecretory maintenance treatment beyond ulcus healing and eradication of Helicobacter pylori infection is only indicated in risk groups. Patients with gastric ulcer caused by NSAID use are managed with antisecretory therapy.

Female↗

PubMed1998

[The enterochromaffin-serotonin system and Helicobacter infection in the mechanisms of the staged development of peptic ulcer].

Submitted in this article are scientific propositions and problems concerning the way ulcer disease (UD) of the gastroduodenal system (GDS) develops through its particular stages, and pathosanogenous role which the enterochromaffin-serotonin system (ECSS), a part of the diffusive neuroendocrine APUD-system of the organism, has in it, along with etiopathogenetic role Helicobacter infection plays in the gastroduodenal mucosa (M). Experience gained by the authors with prospective comprehensive evaluation and treatment of 310 patients with chronic gastroduodenitis (CGD), 198 UD GDS patients and 350 of those surgical patients who had undergone resection of the stomach for complicated UD GDS, indicates that all above pathological states share common etiopathogenetic, clinical, histomorphological and microbiological (Helicobacter infection) features, which facts suggest a common pathomorphogenesis of CGD, erosive GD, UD GDS and postgastroresectional UD, and a staged character of erosive-ulcerous transformation in the GDS M, with the hypercoagulative sings being present at the level of hemomicrocirculation. Progressing structural and functional changes in ECSS parallel to stages of development and severity of the UD GDS course suggest their interrelationship to pathosanogenesis during all stages of erosive-ulcerous transformation. At the molecular level, this may reflect directly the course of staged ulceration and a point of activation of processes of physiological defence, this being of diagnostic as well as prognostic value. The enterochromaffin-serotonin conception of pathosanogenesis of staged erosive-ulcerous transformation in GDS M supplements, rather than contradicts to a current infectious Helicobacter hypothesis of ulcerogenesis. Thus, evaluation of ECSS structural and functional status in UD GDS is to be part of a diagnostic algorithm testing severity of the course as well as of a monitoring of treatment and prognostication.

Adult↗