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PubMed1997

Host mechanisms: are they the key to the various clinical outcomes of Helicobacter pylori infection?

It is unclear why Helicobacter pylori produces different diseases in different persons. High and low acid secretion rates probably contribute to duodenal ulceration and gastric carcinogenesis, respectively. Both of these changes seem to be corrected by eradicating Helicobacter pylori. We are therefore exploring the basic mechanisms and asking why patients react differently? Helicobacter pylori products and certain cytokines released in Helicobacter pylori gastritis release gastrin from G-cells but inhibit parietal cells. Also tumour necrosis factor alpha inhibits somatostatin-cells and interleukin 1 beta inhibits enterochromaffin-like cells. The net result is that antral gastritis tends to increase, whilst corpus gastritis tends to decrease acid secretion. Corpus atrophy further lowers acid through loss of parietal cells. Factors postulated to increase corpus gastritis include host genetics, early acquisition of Helicobacter pylori, more aggressive strains, poor general health and diets high in salt or lacking in antioxidant vitamins. Further research should address the interaction of bacterium, host and environment with a view to preventing the serious clinical outcomes.

Cytokines↗
PubMed1997

Effect of Helicobacter pylori eradication on intestinal metaplasia and gastric epithelium proliferation.

Gastric epithelial turnover increase in Helicobacter pylori infection has been demonstrated by interventional and non interventional methods for proliferating cell detection. We have observed a progressive hyperproliferation with the progression of Helicobacter pylori-induced mucosal lesions until the development of intestinal metaplasia. A similar result has been reported in other studies in the succession from normal mucosa to gastric carcinoma even if interventional techniques show less conspicuous differences in comparison to non interventional ones, which give an overestimated picture of proliferation. Later studies show that Helicobacter pylori-related hyperproliferation reverses after eradication. We have observed that this reversibility does not occur in areas of intestinal metaplasia, where the oncoprotein ras p21, involved in early gastric carcinogenesis, is expressed. This finding agrees with that demonstrating that hyperproliferation in intestinal metaplasia or gastric cancer is not affected by Helicobacter pylori. Other oncogenetic changes in intestinal metaplasia (i.e., p53 mutation) may further explain the persistently modified proliferative pattern of the epithelium. Recent studies suggest a lack of reversibility of intestinal metaplasia after Helicobacter pylori eradication, but this problem remains controversial. Our experience suggests that the persistence of the bacterium may increase the extent of this lesion. In conclusion the development of intestinal metaplasia is associated with an impaired regulation of gastric epithelial proliferation. Nevertheless, from the biological point of view, the progression towards carcinoma requires further DNA changes. Moreover, many questions need to be answered in order to establish clear guidelines for the clinical management.

Cell Division↗
PubMed1997

[Frequency of Helicobacter pylori infection in symptomatic patients in Senegal].

This prospective study was carried out in Dakar, Senegal, to assess the prevalence of Helicobacter pylori infection in symptomatic patients undergoing endoscopy and to evaluate the factors of risk for infection by this type of bacteria in the population. From October to December 1995, 134 patients were included in this study and replied to a standardized questionnaire designed to determine socioeconomic level and living conditions. Diagnosis of Helicobacter pylori infection was based on the combined results of the urea breath test (Clo-test) and histological findings. Helicobacter pylori infection was detected in 82.8% of patients with no significant difference according to sex, age, ethnic group, or living environment (urban or rural). The incidence of infection was also the same in all socioeconomic groups. It was already high in the age group between 11 and 20 years (90.9%). Helicobacter pylori was identified in 76.2% of patients with normal endoscopic findings and in 100% presenting ulcers, erosions, or gastritis. This study shows that the incidence of Helicobacter pylori infection is extremely high regardless of socioeconomic level and that infection begins at a young age. These findings are consistent with the poor hygiene of most people in Senegal.

Adolescent↗
PubMed1997

A growing demand for Helicobacter pylori culture in the near future?

Culture is the basic method in bacteriology. It allowed the discovery of Helicobacter pylori. Problems in the culture of this fragile, slow-growing bacterium concern transport and processing in the laboratory, but they can be solved. Culture has a 100% specificity. When performed properly, it has a sensitivity in the range of the other best diagnostic methods for Helicobacter pylori. It allows strain typing and, most importantly, susceptibility testing to antibiotics, because an increased rate of acquired resistance of Helicobacter pylori is currently observed. Culture must be performed in clinical trials, at least when antibiotics, to which Helicobacter pylori may be resistant, are used. In clinical practice, culture and susceptibility testing can generally be restricted to treatment failures. However, it is important to monitor Helicobacter pylori susceptibility to antibiotics at a national or regional level in order to give recommendations for primary treatment.

Anti-Bacterial Agents↗
PubMed1998

Basal and pentagastrin stimulated acid secretion in duodenal ulcer subjects before and after Helicobacter pylori eradication: a 12-month follow-up study.

BACKGROUND: The effect of infection by Helicobacter pylori on gastric physiology in duodenal ulcer subjects is controversial. There is evidence that the infection is associated with abnormalities in gastrin homeostasis. Consistent changes in pentagastrin-stimulated acid secretory status have proved difficult to establish. This may be because patients have been studied too soon after Helicobacter pylori eradication. AIMS: To study the immediate and longer term effect of Helicobacter pylori eradication on basal and pentagastrin-stimulated acid secretion in duodenal ulcer subjects. PATIENTS AND METHODS: Patients with active duodenal ulcer disease were studied. Ulcers were healed with sucralfate 2 g bd or ranitidine 300 mg nocte. Helicobacter pylori eradication was attempted with bismuth-based "Triple Therapy", and the nine patients in whom the organism was successfully eradicated were followed and studied over the 12-month period. Acid secretion was studied at entry (prior to the initiation of therapy), following healing, following eradication and 12 months later. Basal, low dose (0.1 microgram/kg) and high dose (6 micrograms/kg) pentagastrin-stimulated acid secretion was determined. RESULTS: Whilst there was a tendency for basal and low dose-stimulated acid secretion to fall following eradication, in this study only the reduction in high dose-stimulated acid secretion achieved significance following eradication (entry mean = 59.6, post eradication mean = 49.6, p < 0.03). This effect of eradication on high dose pentagastrin-stimulated acid secretion was also seen at the 12-month study (mean = 48.9, p < 0.02 versus entry). CONCLUSION: The findings of this study suggests that maximally stimulated acid secretion is modestly, albeit significantly, reduced following Helicobacter pylori eradication and that this effect persists.

Adult↗
PubMed1998

Strategy for the retreatment of failed Helicobacter pylori eradication therapy: a case series.

BACKGROUND: Helicobacter pylori eradication therapy can be unsuccessful in 5 to 20% of patients. AIM: To investigate the validity of a strategy using triple therapies for the retreatment of patients with eradication failure, avoiding retreatment with antibiotics prone to induce resistance after use in the first treatment. PATIENTS AND METHODS: From a consecutive sampling of 108 patients still Helicobacter pylori-positive after a first course of antibiotic-based treatment, 74 (68.5%) agreed to a second course of triple therapy. Group 1 (N = 17): treatment failures on an imidazole (1)-based therapy were retreated with clarithromycin (C)-based regimen; Group 2 (N = 28): failures on a C-based therapy with an I-based regimen; Group 3 (N = 7): failures on an IC-based therapy using an I-based regimen and Group 4 (N = 22): failures on a non-I/non-C based therapy with either an I-based, C-based or IC-based regimen. The presence of Helicobacter pylori was assessed by histology and the CLO-test at study entry and two months after stopping therapy. RESULTS: Nine patients were withdrawn from the study (12.2%) due to a lack of end point endoscopy. Helicobacter pylori was cured after the second course of therapy in all but seven patients [10.7% failure by Per Protocol analysis, 21.6% by Intention-To-Treat analysis]. No statistically significant differences were found between the four groups (Group 1: 92.9% PP, 76.5% ITT; Group 2: 90.9% PP, 71.4% ITT; Group 3: PP and ITT 85.7%; Group 4: PP and ITT 86.4%). Minor adverse events were experienced in nine, none of whom required withdrawal from the drug therapy. CONCLUSIONS: A second course of triple therapy with alternate antibiotics effectively eradicated Helicobacter pylori, with only very few treatment failures. This suggests that the therapeutic strategy employed may be recommended.

Adult↗
PubMed2006

Protective immunization against "Candidatus Helicobacter suis" with heterologous antigens of H. pylori and H. felis.

"Helicobacter (H.) heilmannii" type 1 colonizes the human stomach. It has been shown to be identical to "Candidatus H. suis", a Helicobacter species colonizing the stomach of more than 60% of slaughter pigs. This bacterium is, until now, not isolated in vitro. The effect of vaccination on "Candidatus H. suis" infection was studied in a mouse model. Mice were vaccinated intranasally or subcutaneously with whole bacterial cell lysate of Helicobacter pylori or Helicobacter felis and subsequently challenge infected with "Candidatus H. suis". Intranasal and subcutaneous immunisation caused a decrease in faecal excretion of "Candidatus H. suis" DNA. Urease tests on stomach tissue samples at 16 weeks after challenge infection were negative in all H. felis intranasally immunized animals and in the majority of the animals of the other immunisation groups. Since PCR on stomach tissue samples at 16 weeks after challenge infection could still detect "Candidatus H. suis DNA" in all immunisation-challenge groups, complete clearance of challenge bacteria was not achieved.

Administration, Intranasal↗
PubMed2001

Frequent molecular identification of Campylobacter but not Helicobacter genus in bile and biliary epithelium in hepatolithiasis.

Bacterial infection of the biliary tree and bile stasis may be causally related to hepatolithiasis, but which bacterial species are involved and their roles in the pathogenesis of hepatolithiasis have not been ascertained. Recently, the Helicobacter genus was detected in human bile and biliary mucosal samples by molecular techniques, and its association with several biliary diseases has been suggested. The Campylobacter genus, which is closely related to the Helicobacter genus, has also recently been identified as causative of human gastrointestinal diseases. This study attempted to elucidate whether Helicobacter and/or Campylobacter bacteria are present in bile samples and biliary mucosal specimens from hepatolithiasis patients and whether they are involved in the pathogenesis of hepatolithiasis. The 16S rRNA gene of the Helicobacter and of the Campylobacter genus was examined by polymerase chain reaction in DNA samples extracted from bile and/or microdissected biliary epithelium from 69 patients with hepatolithiasis and control patients with choledocholithiasis, cholecystolithiasis, and normal gall bladders. The Helicobacter genus was detected in 1 of 8 (13%) biliary epithelial samples in hepatolithiasis and 1 of 10 (10%) bile samples in choledocholithiasis. The Campylobacter genus was detected in 3 of 14 (21%) bile samples and 5 of 8 (63%) epithelial samples in hepatolithiasis, and in 2 of 15 (13%) bile samples and 1 of 8 (13%) epithelial samples in cholecystolithiasis. The detection rate for Campylobacter in biliary epithelium of hepatolithiasis was significantly higher than in the bile or biliary epithelium of control groups (p<0.05). By a phylogenetic analysis based on nucleotide sequences, the Campylobacter genuses detected in hepatolithiasis were clustered with C. rectus or C. showae. The frequent detection of the Campylobacter 16S rRNA gene in bile, and especially in biliary epithelium of hepatolithiasis, suggests a pathogenetic relationship with Campylobacter infection.

Aged↗
PubMed2001

Helicobacter-induced expression of Bcl-X(L) in B lymphocytes in the mouse model: a possible step in the development of gastric mucosa-associated lymphoid tissue (MALT) lymphoma.

Primary gastric mucosa-associated lymphoid tissue (MALT) lymphoma may develop from chronic infection with Helicobacter sp. in the mouse model. The mechanisms of pathogenesis remain unclear. Regulation of B-cell proliferation and death are important features to investigate. Proteins encoded by bcl-2 family genes, e.g., Bcl-X(L), regulate apoptosis; and alterations in the expression of these genes can contribute to the development of cancer. Our aim was to determine the role of Bcl-X(L) in B lymphocytes in the development of gastric MALT lymphoma associated with Helicobacter infection using the BALB/c mouse model. We analyzed 37 animals with Helicobacter-associated MALT (n = 25), low-grade MALT lymphoma (n = 10) and high-grade lymphoma (n = 2), investigating the in vivo distribution of Bcl-X(L) in B cells/B-lymphoma cells using immunohistochemical analysis. In vitro cultivation of B cells/B-lymphoma cells was employed to perform RT-PCR analysis of Bcl-X(L) mRNA expression after cell stimulation with Helicobacter antigen. We found significant Bcl-X(L) protein expression in B lymphocytes within MALT and low-grade MALT lymphoma, whereas there was no and minimal expression, respectively, of Bcl-X(L) in the 2 high-grade MALT lymphoma cases. Expression of bcl-X(L) mRNA in B lymphocytes was up-regulated in vitro upon Helicobacter-antigen stimulation and associated with prolonged cell survival. These findings support the hypothesis that Bcl-X(L) plays a role in the pathogenesis of B-cell MALT lymphoma by providing cell-survival signals and by triggering the acquisition of MALT.

Animals↗
PubMed2006

Helicobacter connections.

After preliminary studies in 1981, Marshall and Warren conducted a study in which the new bacterium Helicobacter pylori was cultured. In that series, 100 % of 13 patients with duodenal ulcer were found to be infected. The hypothesis that peptic ulcer was caused by a bacterial infection was not accepted without a fight. Most experts believed that Helicobacter was a harmless commensal, infecting people who had ulcers for some other reason. In response, Marshall drank a culture of Helicobacter to prove that the bacteria could infect a healthy person and cause gastritis. The truth behind peptic ulcers was revealed; that is, very young children acquired the Helicobacter organism, leading to a chronic infection which caused a lifelong susceptibility to peptic ulcers. Marshall developed new treatments for the infection and diagnostic tests which allowed the hypothesis to be evaluated and proven. After 1994 Helicobacter was generally accepted as the cause of most gastroduodenal diseases including peptic ulcer and gastric cancer. As a result of this knowledge, treatment is a simple procedure, and stomach surgery has become a rarity.

Australia↗
PubMed1996

Morphologic conversion of Helicobacter pylori from bacillary to coccoid form.

The morphologic conversion of Helicobacter pylori from bacillary to coccoid form was studied by microscopy, viable count on agar plates, and bioluminescence assay of bacterial ATP. When morphologic conversion from bacillary to coccoid form was detected by microscopy, the viable counts and the bacterial ATP decreased. No viable count was found after nine days of incubation, but bacterial ATP was still present. In these cultures in which only the coccoid form of Helicobacter pylori was present, there was no accumulation of extracellular ATP, indicating no leaky cells. During the transition phase from the bacillary to the coccoid form of Helicobacter pylori, the addition of fresh medium increased the intracellular ATP 26-fold. The coccoid form of Helicobacter pylori had a 1000-fold lower ATP level per cell compared to the bacillary form, which indicates a decreased metabolic activity in the coccoid form. Addition of fresh medium to the coccoid cultures from days 9 and 10 increased the ATP level twofold. However, no conversion from coccoid to bacillary form was found in these cultures during prolonged incubation in fresh broth for four weeks. Such conversion needs to be demonstrated before it is proven that the coccoid form of Helicobacter pylori is responsible for transmission and relapse of infection.

Adenosine Triphosphate↗
PubMed2005

In vitro anti-Helicobacter pylori action of 30 Chinese herbal medicines used to treat ulcer diseases.

Infection by Helicobacter pylori has been ascertained to be an important etiologic impetus leading usually to chronic active gastritis and gastric ulcer with growing incidences worldwide. Utilizing as the test pathogen a standard and five clinic strains of Helicobacter pylori, the antibacterial action was assessed in vitro with ethanol extracts of 30 Chinese herbal medicines which have been frequently prescribed since ancient times for treating gastritis-like disorders. Among the 30 tested materials, the ethanol extracts of Abrus cantoniensis (Fabaceae), Saussurea lappa (Asteraceae) and Eugenia caryophyllata (Myrtaceae) were strongly inhibitory to all test strains (MICs: approximately 40 microg/ml), and Hippophae rhamnoides (Elaeagnaceae), Fritillaria thunbergii (Liliaceae), Magnolia officinalis and Schisandra chinensis (Magnoliaceae), Corydalis yanhusuo (Papaveraceae), Citrus reticulata (Rutaceae), Bupleurum chinense and Ligusticum chuanxiong (Apiaceae) substantially active with MICs close to 60.0 microg/ml. As to antibacterial actions of the aqueous extracts of the same drugs, those derived from Cassia obtusifolia (Fabaceae), Fritillaria thunbergii and Eugenia caryophyllata were remarkably inhibitory against all the six Helicobacter pylori strains (MICs: approximately 60 microg/ml). The work compared almost quantitatively the magnitude of the anti-Helicobacter pylori actions of the 30 most prescribed gastritis-treating Chinese herbal drugs, and located as well some source plants where potent anti-Helicobacter pylori phytochemicals could be characterized.

Anti-Bacterial Agents↗
PubMed1997

Detection of spiral and coccoid forms of Helicobacter pylori using a murine monoclonal antibody.

Helicobacter pylori is the major cause of gastritis. The aim of this investigation was to develop a specific antibody, which recognizes both coccoid and spiral forms of Helicobacter pylori and to test this antibody on gastric biopsy sections known to harbour coccoid bacteria. Murine monoclonal antibodies against glycine-acid extracts of five strains of Helicobacter pylori were raised. Immunofluorescence and immunoelectron microscopy showed that one antibody of the IgG1 subclass was specific for both the spiral and coccoid forms. It reacted with a 28 kDa protein that was present in all the five strains tested. Using this antibody in an indirect immunofluorescence assay of formalin-fixed antral and corpus biopsy specimens from Helicobacter pylori-associated gastritis patients showed that nine of the nine antral and five of six corpus specimens harboured the coccoid form of Helicobacter pylori. This technique thus provides a rapid and specific detection of both the spiral and coccoid forms.

Antibodies, Bacterial↗
PubMed2002

[Testing a new in-office test for determination of faecal Helicobacter pylori antigen].

BACKGROUND: To date, the search for an in-office reliable test for Helicobacter pylori infection has been unsuccessful. The aim of the present study was to evaluate a new immunocromatographic in-office test using monoclonal antibodies to determine the presence of Helicobacter pylori antigen in faeces (Stick H. pyl, Operon S.A. Zaragoza). We compared its reliability and reproducibility to the currently available test (HpSA, EIA, Premier Platinum HpSA, Meridian Diagnosis Inc, Cincinnati, Ohio). PATIENTS AND METHOD: 71 consecutive dyspeptic patients were enrolled. Helicobacter pylori status was determined by rapid urease test and Giemsa stain of antral biopsy. Patients with a positive result in the two tests were considered as infected and those with a negative result in both tests were regarded as not infected. Faecal Helicobacter pylori antigen was tested twice by means of HpSA. Four consecutive determinations of Stick H. pyl were also performed. We calculated sensitivity, specificity and positive and negative predictive values of each determination. Concordance between determinations was estimated by the kappa statistics. RESULTS: Forty-eight of 68 patients were infected by Helicobacter pylori. Sensitivity, specificity and positive and negative predictive values were 89-96%, 60-70% 85-88% and 74-87%, respectively, for Stick H. pyl and 70-75%, 60-85%, 85-92% and 55-80%, respectively, for HpSA. Correlation coefficients were 0.82-0.93 for Stick H. pyl and 0.57 for HpSA. CONCLUSIONS: The new Stick H. pyl test shows excellent sensitivity and reproducibility for diagnosis of H. pylori infection. Its reliability appears to be far better than that of HpSA.

Adolescent↗
PubMedDate not supplied

13C-urea breath test for the diagnosis of Helicobacter pylori infection before treatment: is citric acid necessary?

AIM: 13C-urea breath test is one of the best methods for the diagnosis of Helicobacter pylori infection. Although a citric acid solution is generally used prior to urea intake, the superiority of this strategy has not been sufficiently demonstrated. Thus, our aim was to compare 13C-urea breath test with and without citric acid solution, to evaluate whether 13C-urea breath test can also achieve favourable results when the test meal is omitted. METHODS: 13C-urea breath test with and without citric acid were compared prospectively in 53 subjects without prior Helicobacter pylori eradication therapy prescription. Basal samples and at 15', 30', and 45' after taking 100 mg of 13C-urea were obtained. The gold standard for Helicobacter pylori diagnosis was the 13C-urea breath test result with citric acid at 30', and "Delta Over Baseline" values >5 at that time were considered positive. RESULTS: The prevalence of Helicobacter pylori infection was 68%. Mean Delta Over Baseline values with citric acid at 15', 30' and 45' were: 29.6+/-39, 30.8+/-37 and 24.6+/-27; whereas respective values without citric acid were lower: 14.9+/-22, 12.2+/-17 and 10D+/-13 (p<O. 001 for all comparisons, Wilcoxon test for paired data). Thus, the area under the curve (constructed with Delta Over Baseline values at different times) with citric acid was 85+/- 102, and 37+/-50 without citric acid [p<0.001). Correlation coefficient between Delta Over Baseline values with and without citric acid at 30' was 0.73 (p<0.0001). The percentage of subjects achieving the highest Delta Over Baseline value at 15', 30' and 45' with citric acid was 51%, 30% and 19%, whereas without citric acid it was 51%, 26% and 23% (non-significant differences). The area under receiver operating characteristic curve for 13C-urea breath test without citric acid was: 0.98 at 15', 1 at 30' and 0.97 at 45'. The best cut-off point for 13C-urea breath test without citric acid at 30' was anywhere between 3. 3 and 3.9 (that is, a lower value than that usually considered with citric acid), with 100% (95% confidence interval, 90-100%) sensitivity and 100% [82-100%) specificity CONCLUSIONS: 13C-urea breath test values with citric acid are higher than those obtained without citric acid, although this difference does not imply a diagnostic superiority in untreated patients when considering 13C-urea breath test without citric acid at 30'. Therefore, for the diagnosis of Helicobacter pylori infection in untreated patients, citric acid solution in 13C-urea breath test protocol can be omitted.

Adult↗
PubMed2000

Identification of enterohepatic Helicobacter species by restriction fragment-length polymorphism analysis of the 16S rRNA gene.

BACKGROUND: Restriction fragment-length polymorphism (RFLP) analysis of a 1,200-bp polymerase chain reaction-amplified DNA fragment of gene coding for 16S rRNA was used to generate restriction profiles of 11 enterohepatic Helicobacter spp. isolated from various animals and humans. METHODS: The amplicon from each Helicobacter sp. was digested with four restriction endonucleases: Alu I, Hinf I, Hha I, and Dde I. Alu I digestion produced five patterns that were useful for initial differentiation. RESULTS: Most Helicobacter spp. isolated from rodents had the same RFLP profiles by Alu I digestion (except H. rodentium and H. cholecystus), but they had different RFLP profiles by Hha I digestion. Only H. bilis and "H. rappini" mouse isolates could not be readily distinguished by the polymerase chain reaction-RFLP method. However, these two species can be distinguished using H. bilis specific primers. Some of the Helicobacter spp. have an intervening sequence in their 16S rRNA gene, which changes the RFLP patterns; in these cases, sequencing is the preferred method to make an appropriate diagnosis. CONCLUSIONS: The RFLP method used in this study was straightforward and rapid and should prove useful as an adjunct for identification and classification of multiple enterohepatic Helicobacter spp.

Animals↗
PubMed2001

Classification of a Brevundimonas strain detectable after PCR with a Helicobacter-specific primer pair.

In a study for the isolation of new Helicobacter strains, biopsy samples were taken from the gastric mucosa of dogs and subjected to PCR amplification using a Helicobacter-specific primer pair (H276f and H676r, directed to the 16S rDNA) to identify members of this genus in the specimens. From one Helicobacter positive sample, a bacterial strain was isolated which displayed a characteristic band after PCR amplification with the Helicobacter-specific primer pair. The isolate designated H2/98-FUNDUS was motile, oxidase-, catalase- and aminopeptidase-positive and grew only under microaerophilic conditions at 37 degrees C. The bacterium was classified by a polyphasic approach, including analysis of the isoprenoid quinones, fatty acids, polar lipids and partial 16S rDNA sequence. Analysis of the 16S rDNA sequence (1003 bases) indicated that the strain H2/98-FUNDUS is a member of the genus Brevundimonas and most closely related to Brevundimonas aurantiaca DSM 4731T (99.5% sequence similarity). Isolate H2/98-FUNDUS contained a predominant ubiquinone Q-10 and a fatty acid profile with the major compounds C18:1 and C16:0. In the polar lipid extract, phosphatidylglycerol, six unknown phospholipids, one unknown phosphoglycolipid, two unknown glycolipids and two unknown aminolipids were detected. All these results indicate that H2/98-FUNDUS represents a new member of the genus Brevundimonas which gives a positive signal upon PCR employing the Helicobacter-specific primer pair.

Base Sequence↗
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↗