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At least 19 recordsLinked to original sources
PubMed2000

In vivo disruption of the fas pathway abrogates gastric growth alterations secondary to Helicobacter infection.

Helicobacter infection is associated with gastric cell growth alterations, plausibly predisposing to ulcer disease and gastric adenocarcinoma. Previous investigations from our laboratory have implicated the involvement of the Fas pathway in Helicobacter-induced apoptotic signaling in vitro. In this report we use C57BL/6J00064 mice to examine the direct role of Fas signaling in Helicobacter-mediated growth alterations in vivo. Helicobacter infection up-regulated gastric cell Fas antigen (Fas Ag) mRNA and increased surface receptor expression, along with concomitant altered apoptotic and proliferative response, measured by terminal deoxytransferase-deoxyuridine 5'-triphosphate nick end labeling and 5-bromo-2'-deoxuridine immunohistochemistry, respectively. In addition, histopathological alterations, including parietal cell loss and gastric atrophy, were noted. In contrast, infection in B6. MRL-FAS(lpr), a Fas Ag knockout mouse in the C57BL/6 background, did not result in increased apoptosis, proliferation, or histological alterations, a finding that argues strongly for the role of Fas-signaling pathway in orchestrating diverse growth responses to Helicobacter infection.

Animals↗
PubMed1999

Immunomodulation of helicobacter infection.

Helicobacter pylori leads to a chronic infection in humans that is associated with gastric inflammation and a vigorous immune response. Despite the humoral and cellular responses that can be detected in both human and animal models of helicobacter infection, the immune response fails to eliminate the organism. Eradication failure may be due to the niche in which H pylori confines itself, well away from direct contact with elements of the immune system. Alternatively, the general tendency of the intestinal immune response to down- regulate reactivity to noninvasive luminal bacteria also may contribute to the failure to eliminate helicobacter infection. Results of vaccine studies in mouse models indicate that modulating the helper T cell response from a T helper cell type 1 to a T helper cell type 2 response likely is required for the prevention and elimination of helicobacter infection. Understanding the mechanisms by which the immune response controls bacterial infections will allow for the design of novel strategies of immune modulation and the development of vaccines for both the treatment and prevention of H pylori.

Animals↗
PubMed1996

History of Helicobacter infection.

Helicobacter pylori infection is now recognized as the cause of most cases of chronic gastritis, and a major causal factor in peptic ulcer disease. However, though the presence of intragastric bacteria has been recognized for many years, the connection between H. pylori and peptic ulcers has only been established during the last decade. Pathological studies have suggested that intragastric bacteria damage the gastric mucosa, reducing its resistance to acid, while epidemiological studies have suggested that a non-physiological factor, such as bacterial infection, is involved in the development of peptic ulcer. Subsequently, H. pylori, associated with chronic gastritis, was identified in gastric biopsies from patients with peptic ulcer. Eradication of H. pylori has been shown to reduce the recurrence of peptic ulcer after ulcer healing, and such treatment is now widely accepted.

Helicobacter Infections↗
PubMed1997

Extraintestinal pathology associated with Helicobacter infection.

Helicobacter pylori appears to be the most important cause of gastritis and gastric and duodenal ulcer. Its eradication, in fact, promotes healing of these diseases and significantly reduces ulcer recurrence. In the last few years, moreover, besides a local tissue damage, an association between H. pylori infection and various extraintestinal pathologies has also been described. The presence of more toxic strains of H. pylori and the multiplicity of the substances produced, directly or indirectly, in response to the bacterium, besides a genetic predisposition of the individual, are all factors which may enhance the ability of Helicobacter to generate both local and systemic damage.

Bacterial Toxins↗
PubMed2002

Are goats naturally resistant to gastric Helicobacter infection?

Gastric Helicobacter species are widespread and have been reported in wild and domestic mammals of different dietary habits such as humans, dogs, cats, macaques, mice, cheetahs, ferrets, swine and cattle. All have been associated with gastric pathologies. Recently, gastric Helicobacter species were shown to be widespread in cattle and swine in Europe, and there is a report of Helicobacter pylori in sheep in Italy. However, there are no reports of Helicobacter infection in the goat, another important domestic animal of human consumption. The aim of our study was to assess whether Helicobacter abomasal infection was common in goats slaughtered for human consumption. Infection was detected through PCR analysis of DNA extracted from gastric biopsies, using genus- and species-specific primers. Bovine and porcine gastric samples were also analyzed as positive controls. None of the 70 goats were positive for Helicobacter spp.; however, Candidatus Helicobacter bovis and Candidatus Helicobacter suis were detected in 85% of the bovine and 45% of the porcine samples, respectively. We discuss the possibility that goats may exhibit natural resistance to abomasal infection by Helicobacter spp.

Abomasum↗
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↗
PubMed1999

Antibody-independent protective mucosal immunity to gastric helicobacter infection in mice.

Helicobacter pylori infection of the gastric mucosa can result in gastritis and peptic ulcer disease. Although vaccination can induce protective immunity in animal models of Helicobacter infection, the mechanism(s) of protective immunity has not been fully elucidated. This study was designed to determine whether humoral immune responses are required for protective Helicobacter immunity. IgA-deficient or immunoglobulin-deficient mice were orally immunized against Helicobacter felis and then challenged with live H. felis. Both groups were protected at levels comparable to that of wild-type mice. Additionally, inflammation was equivalent in extent and character between wild-type and antibody-deficient mice. Therefore antibody-independent mechanisms of immunity can protect mice against gastric Helicobacter infection.

Animals↗
PubMed2003

Gastric Helicobacter infection inhibits development of oral tolerance to food antigens in mice.

The increase in the transcellular passage of intact antigens across the digestive epithelium infected with Helicobacter pylori may interfere with the regulation of mucosal immune responses. The aim of this work was to study the capacity of Helicobacter infection to inhibit the development of oral tolerance or to promote allergic sensitization and the capacity of a gastro-protective agent, rebamipide, to interfere with these processes in mice. Oral tolerance to ovalbumin (OVA) was studied in 48 C3H/He 4-week-old mice divided into four groups: (i) OVA-sensitized mice; (ii) OVA-"tolerized" mice (that is, mice that were rendered immunologically tolerant); (iii) H. felis-infected, OVA-tolerized mice; (iv) and H. felis-infected, OVA-tolerized, rebamipide-treated mice. Oral sensitization to hen egg lysozyme (HEL) was studied in 48 mice divided into four groups: (i) controls; (ii) HEL-sensitized mice; (iii) H. felis-infected, HEL-sensitized mice; and (iv) H. felis-infected, HEL-sensitized, rebamipide-treated mice. Specific anti-OVA or anti-HEL immunoglobulin E (IgE) and IgG1/IgG2a serum titers were measured by enzyme-linked immunosorbent assay. Additionally, the capacity of rebamipide to interfere with antigen presentation and T-cell activation in vitro, as well as absorption of rebamipide across the epithelial monolayer, was tested. H. felis infection led to the inhibition of oral tolerance to OVA, but rebamipide prevented this inhibitive effect of H. felis. H. felis infection did not enhance the sensitization to HEL, but rebamipide inhibited the development of this sensitization. Moreover, rebamipide inhibited in a dose-dependent manner antigen presentation and T-cell activation in vitro and was shown to be able to cross the epithelium at a concentration capable of inducing this inhibitory effect. We conclude that H. felis can inhibit the development of oral tolerance to OVA in mice and that this inhibition is prevented by rebamipide.

Administration, Oral↗
PubMed2005

Helicobacter infection, chronic inflammation, and the development of malignancy.

PURPOSE OF REVIEW: Chronic infection with Helicobacter pylori affects approximately half the world and results in malignancy in a small subset of this population. Although the frequency of infection in developed nations is falling with a resultant decline in H. pylori-associated peptic ulcer disease, gastric cancer remains the second major cause of cancer death worldwide, with H. pylori infection being a major attributable factor in the development of gastric cancer. This review provides an update on the pathogenesis of Helicobacter infection, the malignancies associated with infection, and how infection and chronic inflammation may lead to the development of gastric malignancy, emphasizing recent developments in the field, particularly those published in leading journals. RECENT FINDINGS: Recent studies have broadened our understanding of the pathogenesis of chronic inflammation associated with Helicobacter infection, and how chronic inflammation contributes to carcinogenesis. There is also continuing evidence from eradication studies in humans and animal models to support the association of Helicobacter infection with gastric cancer. Although there are some differences in the various human trials, recent studies support the notion that early eradication of infection may prevent the development of malignancy, but once certain events have taken place, the process leading to cancer may not be reversible. Continued research into bacterial and host factors that are associated with an increased risk of the development of gastric cancer have also enhanced our understanding of this field. SUMMARY: The emerging literature has important implications for the understanding of the basic pathophysiology leading to malignancy in chronic H. pylori infection throughout the world. Treatment of infection may be beneficial in preventing the development of cancer in certain settings, and the role of antioxidants and other approaches is promising but requires further study. Findings from the investigation of host and bacterial factors that may predispose to the development of more severe disease manifestations including gastric cancer are also important developments in this area.

Animals↗
PubMed2004

Natural and experimental Helicobacter infections.

Current information about Helicobacter infections in humans and various domestic, wild, and research animal species that have been used or have the potential to be used as animal models of human disease is presented. The Helicobacter genus now includes at least 26 formally named species, with additional novel species in the process of being characterized. The natural history, host range with zoonosis potential, pathology, and diagnostic techniques are presented, along with examples of how Helicobacter infection has interfered with unrelated in vivo research. Current recommendations for deriving and managing helicobacter-free animal colonies for research are provided.

Animals↗
PubMed2006

CD4+ CD25+ regulatory T cells modulate the T-cell and antibody responses in helicobacter-infected BALB/c mice.

Gastric Helicobacter spp. induce chronic gastritis that may lead to ulceration and dysplasia. The host elicits a T helper 1 (Th1) response that is fundamental to the pathogenesis of these bacteria. We analyzed immune responses in Helicobacter-infected, normal mice depleted of CD4+ CD25+ T cells to investigate the in vivo role of regulatory T cells (Tregs) in the modulation of Helicobacter immunopathology. BALB/c and transgenic mice were depleted of CD4+ CD25+ T cells by administration of an anti-CD25 antibody either at the time of infection with Helicobacter or during chronic infection and gastritis. Depletion of CD25+ Tregs prior to and during infection of mice with Helicobacter spp. did not affect either bacterial colonization or severity of gastritis. Depletion of CD25+ Tregs was associated with increased Helicobacter-specific antibody levels and an altered isotype distribution. Paragastric lymph node cells from CD25+ Treg-depleted and control infected mice showed similar proliferation to Helicobacter antigens, but only cells from anti-CD25-treated animals secreted Th2 cytokines. CD25+ Tregs do not control the level of gastritis induced by gastric Helicobacter spp. in normal, thymus-intact BALB/c mice. However, CD25+ Tregs influence the cytokine and antibody responses induced by infection. Autoimmune gastritis is not induced in Helicobacter-infected mice depleted of CD25+ Tregs but is induced in CD25+ Treg-depleted mice, which have a higher frequency of autoreactive T cells.

Animals↗
PubMed2001

Helicobacter infection and phospholipase A2 enzymes: effect of Helicobacter felis-infection on the expression and activity of sPLA2 enzymes in mouse stomach.

The murine gastric mucosa possesses very high secretory type phospholipase A2 activity. Northern and Western blots indicated that the pancreatic-type, sPLA2-IB represents the predominant form of sPLA2 enzymes present in the gastric mucosa. Both sPLA2-IB mRNA and protein in the gastric mucosa exceeded levels found in the pancreas, and in contrast to the pancreatic enzyme it was present primarily in the active state. The sPLA2-IB gene is not expressed in the murine small intestine and colon. Infection by the gastritis-inducing bacteria, Helicobacterfelis (H. felis) dramatically and time dependently decreased the PLA2 activity in the glandular stomach of the mouse strain, C57BL/6, sensitive to the organism, which appeared to be related to a decrease in the percentage of sPLA2-IB present in the active form. This bacterial-induced reduction in PLA2 activity was not observed in BALB/c mice that fail to develop gastritis in response to H. felis infection. C57BL/6 mice do not, while BALB/c mice express, the PLA2-II enzyme. The H. felis-induced reduction in sPLA2-IB activity may weaken the gastric barrier by reducing the local concentration of arachidonic and linoleic acid, liberated from membrane phospholipids, the major precursors of 'cytoprotective' prostaglandins. Data presented here suggest that both sPLA2-IB and sPLA2-II enzymes may contribute to the gastric response to Helicobacter infection.

Animals↗
PubMed1998

Clinical significance of Helicobacter infection in children.

Helicobacter pylori infection of the gastric mucosa causes chronic gastritis and is associated with peptic ulcer disease and gastric carcinoma. These are conditions which usually occur in adult life. However, H. pylori is an infection which is mainly acquired in childhood. The overall prevalence of H. pylori in children is 10% in developed countries but can be as high as 30-40% in children from lower socio-economic groups. In developing countries, the prevalence of H. pylori in children ranges from 80-100%. H. pylori gastritis does not appear to be associated with symptoms in children in the absence of duodenal ulcer disease. H. pylori infection is present in the vast majority of children with duodenal ulcer disease and, as in adults, eradication of the organism results in long-term healing of duodenal ulceration. H. pylori infection acquired in childhood is now considered to be a significant risk factor for the development of gastric carcinoma. The World Health Organization has classified H. pylori as a Group 1 carcinogen. Specific epidemiological questions which need to be answered in children include the age at which infection is acquired, specific risk factors for infection, the mode of transmission and the risk of reinfection following treatment. Recently, a one week treatment regimen using colloidal bismuth subcitrate, metronidazole and clarithromycin has been shown to be effective in treating children, but compliance is important. Currently there are no guidelines on the need to treat children and a consensus is urgently required on this issue.

Adolescent↗
PubMed1998

Immunization of BALB/c mice with Helicobacter urease B induces a T helper 2 response absent in Helicobacter infection.

BACKGROUND & AIMS: Infection with Helicobacter induces a T helper type 1 response in mice and humans. Mice can be cured or protected from infection with Helicobacter by mucosal immunization with recombinant H. pylori urease B subunit (rUreB). This study characterizes the immune response of infected mice immunized with rUreB. METHODS: BALB/c mice were infected with H. felis. Two weeks later, they were orally immunized four times with rUreB and cholera toxin (CT) at weekly intervals. Controls were only infected or sham-immunized with CT. Animals were killed at various times after immunization. Splenic CD4(+) cells were obtained and cultured in vitro with rUreB to evaluate antigen-specific proliferation and induction of interferon gamma and interleukin 4 secretion. RESULTS: All rUreB-immunized mice (n = 8) were cured from infection 3 weeks after the fourth immunization. Immunization induced a proliferative response of splenic CD4(+) cells, a progressive decrease in interferon gamma secretion, and a concomitant increase in interleukin 4 secretion after each immunization. A simultaneous increase in rUreB specific serum immunoglobulin G1 levels was observed in infected/immunized mice. CONCLUSIONS: In BALB/c mice, therapeutic mucosal immunization with rUreB induces progressively a Th2 CD4(+) T cell response resulting in the elimination of the pathogen.

Animals↗
PubMed2002

Chinese tea consumption and lower risk of Helicobacter infection.

BACKGROUND: Our first study had shown that Chinese tea has anti-Helicobacter activity. The present study investigated the relationship between patients'Helicobacter status and the history of Chinese tea consumption. METHODS: Chinese patients who had their first upper endoscopy were recruited. Before the procedure, patients completed questionnaires about their current Chinese tea consumption habits and those when they were around 10-25 years old. This information was used to calculate the tea consumption indices (TCI). Gastric biopsies (two from the antrum and two from the corpus) were taken for histological examination for Helicobacter. RESULTS: Eighty patients were recruited. Eight patients were rejected because of either an incomplete questionnaire, absence of gastric biopsy or a suspected history of treatment for Helicobacter infection. Of the 72 patients, 42 (58.3%) were Helicobacter positive. The age, sex ratio and indications for endoscopy were similar in both Helicobacter-positive and -negative groups. Classifying patients using either current, past or total TCI, patients with high tea consumption had significantly lower Helicobacter infection rate than those with low tea consumption (45% compared to 74%, 42% compared to 67% and 40% compared to 83%, respectively). Helicobacter-negative patients had higher overall TCI than Helicobacter-positive patients (28.2:17.3). When current and previous histories were analyzed separately, Helicobacter-negative patients also had a trend towards higher TCI currently (16.6:11.0) and in their 20s (11.6:6.1). CONCLUSIONS: There is a significant inverse relationship between Chinese tea consumption and Helicobacter infection. Chinese tea consumption may decrease the chance of Helicobacter infection.

Adult↗
PubMedDate not supplied

Detection, eradication, and research implications of Helicobacter infections in laboratory rodents.

Researchers first isolated and characterized Helicobacter hepaticus in 1994 as a cause of hepatitis that progressed to hepatocellular carcinoma in A/JCr mice. During the past decade, isolation and characterization of additional novel helicobacters from rodents has continued. In addition to causing overt disease, rodent helicobacter infections are important because intercurrent disease in select models will confound research data. Emerging evidence suggests that inflammatory responses to enterohepatic helicobacter infections may alter host responses to other experimental stimuli in unanticipated ways. Additionally, scientists have experimentally infected a variety of inbred mouse strains and genetically engineered mice with a variety of Helicobacter spp. isolated from rodents, birds, and higher mammals (including humans) to develop animal models of gastrointestinal diseases as well as idiopathic human disease syndromes. This review highlights current information about helicobacter infections in laboratory rodents and provides recommendations for the detection and eradication of these infections. The authors discuss the impact of subclinical and clinical disease and offer recommendations for managing helicobacter-free rodent colonies.

Animals↗
PubMed1996

[Therapy of Helicobacter infection].

Infection with Helicobacter pylori (H.p.) leads to mostly asymptomatic chronic gastritis. However, H.p. plays a role in peptic ulcer, giant fold gastritis (Menetrier's disease), and possibly in gastric carcinoma and low-grade MALT lymphoma. Whether functional dyspepsia also represents a Helicobacter-induced entity is questionable. H.p. should be eradicated in patients with peptic ulcer disease, Menetrier+s disease and - but in controlled studies only - in MALT lymphomas. Triple therapy with low-dose proton pump inhibitors and two antibiotics is the most favourable treatment compared to dual therapy with omeprazole and amoxicillin/clarithromycin despite the unresolved question of the development of drug resistance.

Anti-Bacterial Agents↗
PubMed1993

[Diagnostic criteria of pyloric helicobacter infection in peptic ulcer].

Helicobacter pylori (HP) in 41 patients (10 with stomach ulcer and 31 with duodenum ulcer) was found in gastro-biopsies from the stomach antrum before and after the treatment. The following methods to reveal HP were used: Giemsa staining, immunoperoxidase reaction with polyclonal monospecific antibodies against HP, urease rapid test. HP was also revealed in the blood serum by antibodies against HP by means of enzyme immunoassay. Electron microscopy was performed in 5 patients and bacteriologic study in 10 patients. Immunohistochemical method allows one to judge about real HP colonization of the gastric mucosa. Bacterioscopy with Giemsa staining gives good results but they are not true markers of HP presence this being explained by other methods. Serologic enzyme immunoassay gives an idea about the patient contamination, but not about HP eliminations as a result of treatment. Urease-test is adjuvant.

Azure Stains↗