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PubMed1998

Mucosal and systemic antibody levels against Helicobacter pylori do not parallel gastric inflammatory changes.

BACKGROUND AND AIMS: Mucosal and systemic antibodies against Helicobacter pylori have been detected but their role in the natural history of Helicobacter pylori-related diseases is unclear. In this study, the levels of Helicobacter pylori IgG and IgA were related to the grade of gastritis. PATIENTS AND METHODS: A series of 152 dyspeptic patients underwent gastroscopy with biopsies. Helicobacter pylori was detected in 131 (86%) patients. Samples of serum and unstimulated saliva were collected. Helicobacter pylori IgG and IgA were measured in homogenised gastric biopsies, saliva and serum by an in-house enzyme linked immunosorbent assay. RESULTS: Levels of gastric mucosa, salivary and serum Helicobacter pylori IgG were higher (p < or = 0.01) in Helicobacter pylori positive than negative patients. Likewise, levels of gastric mucosa and serum Helicobacter pylori IgA were higher (p < 0.01) in Helicobacter pylori positive patients. Gastric mucosa, saliva and serum Helicobacter pylori antibody levels did not differ between superficial and atrophic, active and inactive Helicobacter pylori positive gastritis. CONCLUSIONS: These data indicate that gastric inflammatory changes may not necessarily be related to the antibody response against Helicobacter pylori.

Adult↗
PubMed1999

Comparison of iron uptake in different Helicobacter species.

Comparison of iron uptake of four Helicobacter species (Helicobacter pylori, Helicobacter felis, Helicobacter acinonyx, and Helicobacter mustelae), associated with various degrees of gastritis in their respective host, with five other species which colonize the intestinal tract of various animals (Helicobacter fennelliae, Helicobacter cinaedi, Helicobacter muridarum, Helicobacter bilis, and Helicobacter hepaticus), demonstrated that the iron acquisition system differed according to the ecological niche of the organism. Gastric Helicobacter, except for H. pylori, which used iron from human lactoferrin, were nonsiderophore-producing organisms and were only able to obtain iron from heme and hemoglobin. Nongastric Helicobacter produced siderophores and were able to use for growth a wide range of iron sources (bovine and human lactoferrin and transferrin, heme, hemoglobin).

Animals↗
PubMed1996

Effect of specimen collection techniques, transport media, and incubation of cultures on the detection rate of Helicobacter pylori.

Culture and histologic examination are considered "gold standard" methods for the detection of Helicobacter pylori, but discrepancies may occur with either method. Failure to detect Helicobacter pylori may be due to sampling error, inappropriate transport or culture media, or insufficient duration of the incubation period. Rates of detection of Helicobacter pylori by culture and histopathologic examination of gastric mucosal biopsy specimens were determined in 102 consecutive dyspeptic patients. In a separate group of 60 patients, rates of detection of Helicobacter pylori by culture of antral brushings and the length of incubation required in selective and nonselective culture media were studied. In the first group of 102 patients, the combination of culture and histologic examination detected 54 Helicobacter pylori-positive patients, whereas the separate techniques each detected 51 Helicobacter pylori-positive patients. In the second group of 60 patients evaluated by culture of antral brushings, the rate of detection of Helicobacter pylori was 25 of 60 and was similar for culture (25/60) and histologic examination (25/60). In the second group the length of incubation required to detect Helicobacter pylori was different for selective and nonselective media. In nonselective media, incubation of up to ten days was required to detect all Helicobacter pylori infections, whereas in selective media seven days was sufficient. Rates of detection of Helicobacter pylori by culture, histopathologic examination and culture from brushings were similar, whereas the combination of culture and histopathologic examination achieved a superior rate of detection. The incubation period required for the detection of Helicobacter pylori by culture was a minimum of seven days and was dependent on the culture medium used.

Adult↗
PubMed1999

Occurrence and characterization of gastric Helicobacter spp. in naturally infected dogs.

Helicobacter-like organisms are frequently observed in the stomach of dogs but the relationship between these microorganisms and gastric pathology has not been clearly established. Different species of helicobacters are known to be present in the canine stomach but their specific prevalence in naturally infected dogs is unknown. The aims of this study were to isolate and characterize helicobacters in canine gastric biopsies, to compare the commonly used tests for the identification of Helicobacter spp. and to determine the occurrence of these species in dogs. Twenty-three out of 25 dogs (92%) were positive for Helicobacter-like organisms in cytological screening. Culture was successful from biopsies of 5/25 dogs. The isolates were analyzed by electron microscopy, biochemical and physiological tests, whole protein analysis and 16S rDNA sequencing. Helicobacter felis was identified in four samples and Helicobacter bizzozeronii in one sample. Only the whole protein analysis in combination with electron microscopy was able to clearly discriminate the two species. Compared to the high prevalence of Helicobacter-like organisms, the occurrence of H. felis and H. bizzozeronii, was low (17 and 4%, respectively). No Flexispira rappini-like organisms or H. salomonis were detected. Electron microscopy revealed that H. bizzozeronii-like microorganisms were present in three additional biopsies where we were unable to culture any Helicobacter-like organisms. These observations indicate that in the stomach of dogs not all helicobacters are culturable. The unculturable bacteria appeared to be the prevalent ones and may represent different spiral organisms. The presence of distinct helicobacters with different characteristics can reflect different roles in the pathogenesis of canine gastric disease.

Animals↗
PubMed2000

Cure of Helicobacter pylori-positive active duodenal ulcer patients: a double-blind, multicentre, 12-month study comparing a two-week dual vs a one-week triple therapy. GISU (Interdisciplinary Group for Ulcer Study).

AIMS: To compare a two-week dual therapy to a one-week triple therapy for the healing of duodenal ulcer and the eradication of the Helicobacter pylori infection. PATIENTS AND METHODS: A total of 165 patients with active duodenal ulcer were enrolled in the study. At entry, endoscopy, clinical examination and laboratory tests were performed. Histology and the rapid urease test were used to diagnose Helicobacter pylori infection. Patients received either lansoprazole 30 mg plus amoxycillin 1 g bid for two weeks (two-week, dual therapy) or lansoprazole 30 mg plus amoxycillin 1 g plus tinidazole 500 mg bid for one week plus lansoprazole qd for an additional week (one-week, triple therapy). Two and twelve months after cessation of therapy, endoscopy and clinical assessments were repeated. RESULTS: Duodenal ulcer healing and Helicobacter pylori eradication were both significantly greater (p<0.0001) in the triple therapy group (healing: 98.6%; Helicobacter pylori cure rate: 72.6%) than in the dual therapy group (healing: 77.3%; Helicobacter pylori cure rate: 33.3%). Ulcers healed more frequently in Helicobacter pyloricured than in Helicobacter pylori-not cured patients (94.9% vs. 77.2%; p<0.0022). After one year, Helicobacter pylori eradication was re-confirmed in 46/58 patients previously treated with the triple therapy and in 10/40 patients treated with the dual therapy [p<0.0001]. Only three duodenal ulcer relapses were observed throughout follow-up: all were in Helicobacter pylori-not cured patients. CONCLUSIONS: Triple therapy was more effective than dual both in curing Helicobacter pylori infection and healing active duodenal ulcers. The speed of ulcer healing obtained after only 7 days of antibiotics and 14 days of proton pump inhibitors confirmed that longer periods of anti ulcer therapy were not necessary. Helicobacter pylori -not cured patients had more slowly healing ulcers which were more apt to relapse when left untreated.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed2001

Coinfection of enteric Helicobacter spp. and Campylobacter spp. in cats.

During a 6-year period, 64 of 227 commercially reared cats had microaerobic bacteria isolated from their feces. All the isolates were initially identified as Campylobacter-like organisms based on biochemical and phenotypic characteristics. DNA extractions from 51 of these isolates were subjected to PCR using primers specific for Helicobacter spp. and Campylobacter spp. Of the isolates, 92% (47 of 51 isolates) were positive for Campylobacter spp., 41% (21 of 51 isolates) were positive for Helicobacter spp., 33% (17 of 51 isolates) were positive for both genera, 59% (30 of 51 isolates) were positive only for Campylobacter spp., and 8% (4 of 51) were positive only for Helicobacter spp. Sixteen of the 47 Campylobacter-positive cultures were positive for more than one Campylobacter spp. Based on a species-specific PCR assay, 83% of the isolates were identified as Campylobacter helveticus, 47% of the isolates were identified as Campylobacter upsaliensis, and 6% of the isolates were classified as Campylobacter jejuni. The 1.2-kb PCR products of the 16S rRNA genes of 19 Helicobacter species isolates were subjected to restriction fragment length polymorphism (RFLP) analysis. Of the five different RFLP patterns obtained, two clustered with Helicobacter ("Flexispira") taxon 8, one clustered with Helicobacter bilis, one clustered with Helicobacter canis, and the remaining pattern was closely related to a novel Helicobacter sp. strain isolated from a woodchuck. The sequence data for the 16S rRNA genes of 10 Helicobacter spp. validated the RFLP-based identification of these isolates. This study demonstrated that biochemical and phenotypic characteristics of microaerobic organisms in cat feces were insufficient to characterize mixed Helicobacter and Campylobacter infections. Molecular structure-based diagnostics using genus- and species-specific PCR, RFLP analysis, and 16S rRNA sequence analysis enabled the identification of multiple microaerobic species in individual animals. The clinical relevance of enteric Helicobacter and Campylobacter coinfection in cats will require further studies.

Animals↗
PubMedDate not supplied

Role of Helicobacter pylori in gastric carcinoma.

BACKGROUND: Helicobacter pylori infection has recently been incriminated in the pathogenesis of gastric carcinoma and chronic atrophic gastritis and intestinal metaplasia are considered to be precursors of this condition. Although the incidence of Helicobacter pylori infection in India is high that of gastric carcinoma is low. We, therefore, decided to examine the association between Helicobacter pylori, intestinal metaplasia and gastric carcinoma in a prospective study. METHODS: Fifty patients with carcinoma of the stomach and 50 with non-ulcer dyspepsia underwent upper gastro-intestinal endoscopy and had biopsies from the antrum, body and carcinomatous tissue. In 12 cases of gastric carcinoma, tissue was obtained from resected specimens at operation. The types of gastritis, intestinal metaplasia and presence of Helicobacter pylori were assessed by staining with haematoxylin and eosin, periodic acid-Schiff reagent with alcian blue and Warthin-Starry stains. RESULTS: The incidence of chronic atrophic gastritis, intestinal metaplasia and Helicobacter pylori were 82%, 36% and 38% in patients with carcinoma and 86%, 4% and 68% in those with non-ulcer dyspepsia. Helicobacter pylori positivity was significantly higher (p < 0.05) and intestinal metaplasia significantly lower (p < 0.001) in patients with non-ulcer dyspepsia than in those with carcinoma. Of the 50 cases with carcinoma, 28 were of the intestinal and 22 of the diffuse type. The incidence of chronic atrophic gastritis, intestinal metaplasia and Helicobacter pylori in the intestinal type of carcinoma was 71%, 46% and 39% while in the diffuse type it was 32%, 23% and 36%. The incidence of Helicobacter pylori infection did not differ significantly in the two types of carcinoma. CONCLUSIONS: We have found that although Helicobacter pylori infection and chronic atrophic gastritis are common in Indians, the incidence of intestinal metaplasia is low. Helicobacter pylori infection was equally common in both the intestinal and diffuse type of gastric carcinomas. Our findings, therefore, cast doubt on the role of Helicobacter pylori infection in gastric carcinogenesis.

Adult↗
PubMed1997

Helicobacter pylori eradication may reduce the risk of gastroduodenal lesions in chronic NSAID users.

Helicobacter pylori and non-steroidal anti-inflammatory drugs are two of the most common causes of peptic ulceration. The aim of this review is to assess the possible inter-relationships between Helicobacter pylori and non-steroidal anti-inflammatory drugs in the pathogenesis of gastric and duodenal erosions and ulcers, with the aim of assessing if the presence of Helicobacter pylori is likely to increase the likelihood of non-steroidal anti-inflammatory drug-related gastroduodenal symptoms and lesions, and if eradication of Helicobacter pylori may reduce or prevent non-steroidal anti-inflammatory drug lesions. There appears to be more likelihood of dyspeptic symptoms in patients on long-term non-steroidal anti-inflammatory drugs when Helicobacter pylori is present. The balance of evidence also suggests that peptic ulcers and erosions in patients on long-term non-steroidal anti-inflammatory drugs may be more likely to occur in patients who are Helicobacter pylori positive compared to those who are Helicobacter pylori negative. Although Helicobacter pylori and non-steroidal anti-inflammatory drugs both increase the risk of peptic ulcer bleeding, the risk does not appear to be additive. There is increasing evidence from prospective studies that eradication of Helicobacter pylori may reduce the incidence of ulcers in patients on non-steroidal anti-inflammatory drugs. More prospective long-term studies are required. If Helicobacter pylori is confirmed to be a factor in this respect, it will aid in the targeting of patients at greatest risk of developing ulcers in patients on long-term non-steroidal anti-inflammatory drugs. Those at greatest risk are elderly patients, especially females, smokers, patients with a previous ulcer history, severe or debilitating arthritis or who have other chronic diseases. The addition of Helicobacter pylori to this list and its subsequent eradication may improve the outlook for these patients and help in the effective targeting of patients at greatest risk who are on long-term non-steroidal anti-inflammatory drugs.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1998

Helicobacter pylori and the liver: any relationship?

Helicobacter pylori infection is being correlated to a number of human diseases, among which also those of the liver. From a clinical point of view, 4 "areas of interest" for the suggested correlation can be identified: 1. Helicobacter pylori and portal hypertension-related congestive gastropathy in cirrhotics. There are, in the literature, at least 7 studies confirming that the microorganism has no role in causing or worsening the disease. 2. Helicobacter pylori and duodenal ulcer in cirrhotic patients. Apparently, in the cirrhotic patient, the microorganism has no role in causing duodenal ulcer. 3. Helicobacter pylori, ammonia production and hepatic encephalopathy. In this case, there are at least three studies showing that Helicobacter pylori infection increases the risk of developing encephalopathy in the cirrhotic patient, this being a somewhat expected finding. 4. Helicobacter pylori infection in chronic liver disease and its diagnosis. Evidence in the literature suggests: a) that hypertensive gastropathy might not represent a favourable environment for Helicobacter pylori thus making the diagnostic sensitivity of the biopsy lower than expected, and b) that even serological diagnosis might provide data of difficult interpretation, as shown in non alcoholic cirrhosis and, by our own group, in primary biliary cirrhosis. More intriguing are the data generated with respect to the potential capacity of Helicobacter pylori and Helicobacter pylori-like bacteria such as, in particular, Helicobacter hepaticus to damage the liver by producing toxins with a granulating effect on liver cell lines which, in vivo, through the portal tract, might reach the liver, thus causing hepatocellular damage. The point has been addressed by a number of investigators and autoimmune mechanisms have also been suggested. In summary, from the clinical point of view, some evidence suggests that Helicobacter pylori infection might be relevant in the pathogenesis of hepatic encephalopathy in cirrhosis. The data being generated with respect to a direct hepatotoxicity are, at present, stimulating but only speculative.

Ammonia↗
PubMed2001

Helicobacter pylori and tonsillectomy.

Tonsillar tissue is a component of mucosa-associated lymphoid tissue (MALT), which has evolved to protect vulnerable mucosal surfaces. Helicobacter pylori, implicated as an aetiological factor in duodenal ulcers and gastritis, induces the appearance of lymphoid aggregates (MALT) in the stomach. This organism is cytotoxic via a nitric oxide synthase cascade. The possibility that tonsillar tissue processes Helicobacter pylori or that Helicobacter pylori can colonize the palatine tonsils is explored. The study design was that of a prospective study. We determined if Helicobacter pylori (i) forms part of the normal microenvironment of the tonsil, (ii) plays a role in the pathogenesis of tonsillitis and (iii) is associated with increased expression of inducible nitric oxide synthase (iNOS) in macrophages of the tonsil. Serology for Helicobacter pylori was performed on 50 patients undergoing tonsillectomy. Tonsillar specimens were monitored for urease activity by CLO test (a sealed plastic slide holding an agar gel, which contains urea and detects the urease enzyme of Helicobacter pylori), and immunocytochemically probed for Helicobacter pylori and iNOS expression. The mean age of this patient group was 17.2 years (3-36 years). Fourteen (28%) were sero-positive for Helicobacter pylori but no evidence of this pathogen was found in any tonsillar specimen. The number of macrophages staining for iNOS, per field, under a magnification of x40, was increased in sero-positive patients (13.3 +/- 1.3 versus 9.9 +/- 0.7; P = 0.01). Helicobacter pylori does not appear to colonize the tonsil. We believe that Helicobacter pylori primes the tonsils by inducing macrophage iNOS expression. The higher expression in sero-positive patients is a reflection of a pro-inflammatory reaction to Helicobacter pylori that is both local and systemic.

Adolescent↗
PubMed2004

Phylogenetic analysis of gastric and enterohepatic Helicobacter species based on partial HSP60 gene sequences.

Analysis of 16S rRNA gene sequences has been the method generally used to study the evolution and phylogeny of bacteria. Phylogenetic analysis of the 16S rRNA gene has shown the position of the genus Helicobacter in the epsilon-subclass of the Proteobacteria. Because 16S rRNA-based phylogeny does not always correspond to the results of polyphasic taxonomy, and the related species cannot always be separated, new phylogenetic markers for Helicobacter species are needed. In this study, conserved partial (600 bp) 60 kDa heat-shock protein (HSP60) sequences were used to study the phylogeny of 37 strains of gastric and enterohepatic Helicobacter species, including type strains of 15 Helicobacter species with validly published names, reference strains of flexispira taxa and Helicobacter felis, Helicobacter bizzozeronii and Helicobacter salomonis and canine flexispira strains. The partial HSP60 gene sequence proved to be a useful phylogenetic marker for the genus Helicobacter, providing a means of differentiating all 15 Helicobacter species analysed. In the resulting phylogenetic tree, gastric Helicobacter species and enterohepatic species with flexispira morphology formed tight, separate clusters. In general, HSP60 sequence similarities between Helicobacter species were significantly lower than the corresponding 16S rRNA gene sequence similarities, indicating a better resolution for species identification. In addition, a specific PCR method for identifying H. salomonis was developed based on the partial HSP60 sequence.

Animals↗
PubMed2004

High prevalence of Helicobacter Species detected in laboratory mouse strains by multiplex PCR-denaturing gradient gel electrophoresis and pyrosequencing.

Rodent models have been developed to study the pathogenesis of diseases caused by Helicobacter pylori, as well as by other gastric and intestinal Helicobacter spp., but some murine enteric Helicobacter spp. cause hepatobiliary and intestinal tract diseases in specific inbred strains of laboratory mice. To identify these murine Helicobacter spp., we developed an assay based on PCR-denaturing gradient gel electrophoresis and pyrosequencing. Nine strains of mice, maintained in four conventional laboratory animal houses, were assessed for Helicobacter sp. carriage. Tissue samples from the liver, stomach, and small intestine, as well as feces and blood, were collected; and all specimens (n = 210) were screened by a Helicobacter genus-specific PCR. Positive samples were identified to the species level by multiplex denaturing gradient gel electrophoresis, pyrosequencing, and a H. ganmani-specific PCR assay. Histologic examination of 30 tissue samples from 18 animals was performed. All mice of eight of the nine strains tested were Helicobacter genus positive; H. bilis, H. hepaticus, H. typhlonius, H. ganmani, H. rodentium, and a Helicobacter sp. flexispira-like organism were identified. Helicobacter DNA was common in fecal (86%) and gastric tissue (55%) specimens, whereas samples of liver tissue (21%), small intestine tissue (17%), and blood (14%) were less commonly positive. Several mouse strains were colonized with more than one Helicobacter spp. Most tissue specimens analyzed showed no signs of inflammation; however, in one strain of mice, hepatitis was diagnosed in livers positive for H. hepaticus, and in another strain, gastric colonization by H. typhlonius was associated with gastritis. The diagnostic setup developed was efficient at identifying most murine Helicobacter spp.

Animals↗
PubMed1992

Modes of Helicobacter colonization and gastric epithelial damage.

A total of 144 gastric biopsies colonized by Helicobacter-like organisms were studied under light and differential interference contrast microscopy for the modes of bacterial colonization. Biopsies were also graded for the degree of epithelial damage (epithelial-damage-grade: 0 to 6, in ascending order of severity) and density of Helicobacter-like organism (Helicobacter-grade: 0 to 6, in ascending order of bacterial density). Three modes of colonization were identified: free-in-mucus, surface-adhesion and intercellular colonization. Because light microscopy cannot definitely prove the presence of intracellular colonization, bacteria located between cells and below the apical cell border were counted together as intercellular colonization. Bacteria free-in-mucus were seen in all biopsies. Surface adhesion was seen in 50-87.9% of biopsies, without obvious correlation with the epithelial-damage- and Helicobacter-grades. The incidences of intercellular and intracellular colonization were directly proportional to the epithelial-damage- and Helicobacter-grades. Free-in-mucus as the predominant mode of colonization was mainly seen in biopsies with lower (1-3) epithelial-damage- and Helicobacter-grades. Conversely, biopsies with intercellular colonization as the predominant mode of colonization were mainly cases with higher (4-6) epithelial-damage- and Helicobacter-grades. In cases showing predominantly bacteria between cells, 69.2% had a gastric ulcer whereas only 38.8% of cases showing predominantly bacteria free-in-mucus showed ulceration (P < 0.01). These results indicate that Helicobacter-like organisms can invade and penetrate between epithelial cells. When free-in-mucus, Helicobacter-like organisms are less likely to induce epithelial damage. However, the more invasive modes of colonization (intercellular) were associated with severe epithelial damage and high Helicobacter density.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2005

Identification of non-Helicobacter pylori spiral organisms in gastric samples from humans, dogs, and cats.

Tightly coiled bacteria are a rare cause of gastric pathology in humans and represent a mixture of species for which a zoonotic origin is suspected. Similar organisms are common inhabitants of the gastric mucosae of carnivores and pigs. It was the goal of the present study to determine the actual occurrence of each individual Helicobacter species in human, canine, and feline stomachs in order to better understand the possible zoonotic significance. Gastric biopsy samples from humans with histological evidence of non-Helicobacter pylori spiral bacteria (n = 123) and samples from the gastric antrum, corpus, and cardia from dogs (n = 110) and cats (n = 43) were subjected to a multiplex PCR, enabling the identification of Helicobacter felis, Helicobacter bizzozeronii, Helicobacter salomonis, and "Candidatus Helicobacter suis." A PCR for detecting H. pylori was applied to all human samples. Single infections with "Candidatus Helicobacter suis," H. felis, H. bizzozeronii, H. salomonis, a hitherto unknown genotype of a non-H. pylori spiral organism (Helicobacter-like organism 135 [HLO135]), and H. pylori were identified in 30.9%, 8.9%, 2.4%, 11.4%, 7.3%, and 8.9% of the human biopsy samples, respectively. Mixed infections (16.3%) with two or even three of these were also found. In the canine stomach, H. bizzozeronii (70.0%) was encountered as the main spiral organism, while H. felis (62.7%) and HLO135 (67.4%) were the predominant Helicobacter species found in the feline gastric mucosa. Although the majority of human non-H. pylori organisms are Helicobacter species naturally occurring in the stomachs of pigs, cats, and dogs, the frequent identification of H. salomonis in human gastric biopsy samples is in contrast to its rare identification in pet carnivore samples, urging us to suspect other sources of infection.

Animals↗
PubMed1996

Helicobacter pylori infection enhances mucosal interleukin-1 beta, interleukin-6, and the soluble receptor of interleukin-2.

It is thought that Helicobacter pylori colonization of the gastric mucosa might stimulate the production of several cytokines, which might trigger and maintain the gastric inflammation associated with Helicobacter pylori infection. In the present study we evaluated interleukin-1 beta. interleukin-6, and the soluble receptor of interleukin-2 both in mucosal homogenates and in the sera of Helicobacter pylori-infected (39 cases) and uninfected (40 cases) patients to investigate whether there was any relationship between variations in cytokines and (1) the severity of Helicobacter pylori-associated gastritis or (2) CagA-positive Helicobacter pylori strains. Mucosal, but not serum levels of interleukins-1 and -6 and interleukin-2 receptor were significantly higher in infected than uninfected patients. Serum levels of Helicobacter pylori antibodies were significantly higher in infected than uninfected patients. These levels correlated with mucosal interleukin-1 beta. The degree of antral or body inflammatory grade was higher in infected than in uninfected patients; cytokines levels were higher in patients with high-grade gastritis, most of whom were Helicobacter pylori positive. Patients infected with CagA-positive strains also had higher levels of interleukin-1 beta, but not of interleukin-2 receptor or interleukin-6. In conclusion. Helicobacter pylori infection results in a local increase in interleukins-1 beta and -6 and interleukin-2 receptor associated with high-grade mucosal inflammation. Interleukin-1 beta seems to favor anti-Helicobacter pylori antibody production, and mucosal levels are enhanced mainly in patients infected with cytotoxic Helicobacter pylori strains.

Adult↗
PubMed1997

Seroprevalence and epidemiology of Helicobacter pylori infection in patients with cirrhosis.

BACKGROUND: Helicobacter pylori infection is the major pathogenic factor for peptic ulcer disease. Its epidemiology is not fully known; few data are available in patients with chronic liver disease. AIMS: To investigate the seroprevalence and factors associated with Helicobacter pylori infection in a series of liver cirrhosis patients. METHODS: Two hundred and twenty consecutive patients were prospectively included in a study aimed to evaluate the effect of dietary intervention on cirrhosis complications and survival. At inclusion, an epidemiological and clinical questionnaire was completed. Sera were obtained and stored at -70 degrees C until analyzed. They were tested for Helicobacter pylori antibodies using a commercial ELISA kit. RESULTS: Eleven out of 220 patients had borderline anti-Helicobacter pylori IgG titers. Of the remaining 209 patients, 105 (50.2%) showed positive titers of Helicobacter pylori IgG. Univariate analysis showed that Helicobacter pylori infection was more frequent in older patients, those born outside Catalonia, and in patients with a low educational level. Past ethanol consumption and current smoking correlated negatively with Helicobacter pylori infection. Multivariate analysis selected age (OR 3.1. 95% CI 1.46-6.45), educational level (OR 2.2. 95% CI 1.18-4.2) and alcohol consumption (OR 0.7. 95% CI 0.45-0.99) as the variables independently related to Helicobacter pylori infection. CONCLUSIONS: Helicobacter pylori infection in cirrhosis has the same epidemiological pattern as in the general population. Suggestions that the etiology or the severity of the liver disease could be related to Helicobacter pylori infection were not confirmed by our study.

Adult↗
PubMed2001

Reactive oxygen species activity, mucosal lipoperoxidation and glutathione in Helicobacter pylori-infected gastric mucosa.

BACKGROUND AND AIM: Helicobacter pylori is considered as the major pathogen in Helicobacter pylori-associated gastroduodenal disease, but the mechanism of its action has not been fully explained. This study was performed to assess the reactive oxygen species activity and the damage in Helicobacter pylori-infected gastric mucosa. METHODS: Gastric biopsy specimens were obtained from 308 patients undergoing endoscopy. Gastric mucosal damage was assessed by using luminol enhanced chemiluminescence, thiobarbituric acid-reactive substance, and mucosal glutathione. RESULTS: The chemiluminescence and thiobarbituric acid-reactive substance-equivalent levels in the mucosa of patients with Helicobacter pylori-positive gastric mucosa (43.8 +/- 134.9 c.p.m./microg tissue, 157.0 +/- 96.2 nmol/g tissue, respectively) were significantly higher than in those with Helicobacter pylori-negative mucosa (6.8 +/- 20.3 c.p.m./microg tissue, 110.0 +/- 51.6 nmol/g tissue, respectively; P=0.000, P=0.016, respectively). The glutathione levels in the mucosa of patients with Helicobacter pylori-positive gastric mucosa (159.3 +/- 76.6 nmol/microg tissue) were significantly lower than in those with Helicobacter pylori-negative gastric mucosa (212.3 +/- 134.3 nmol/microg tissue; P=0.008). After the data were divided according to the presence of Helicobacter pylori, there were no significant differences in chemiluminescence, thiobarbituric acid-reactive substance, and glutathione among the different macroscopic findings within Helicobacter pylori-positive and -negative gastric mucosa. CONCLUSIONS: Helicobacter pylori infection plays a pathological role in many gastrointestinal diseases through excessive mucosal-reactive oxygen species production, pronounced membrane damage, and the depletion of gastric anti-oxidants.

Adult↗
PubMed2005

Identification of cholelithogenic enterohepatic helicobacter species and their role in murine cholesterol gallstone formation.

BACKGROUND & AIMS: Helicobacter spp are common inhabitants of the hepatobiliary and gastrointestinal tracts of humans and animals and cause a variety of well-described diseases. Recent epidemiologic results suggest a possible association between enterohepatic Helicobacter spp and cholesterol cholelithiasis, chronic cholecystitis, and gallbladder cancer. To test this, we prospectively investigated the effects of Helicobacter spp infection in cholesterol gallstone pathogenesis in the highly susceptible C57L/J mouse model. METHODS: Helicobacter spp-free adult male C57L mice were infected with several different enterohepatic Helicobacter spp or left uninfected and fed either a lithogenic diet or standard mouse chow for 8 and 18 weeks. At the conclusion of the study, bile was examined microscopically and diagnostic culture and polymerase chain reaction were performed. RESULTS: Mice infected with Helicobacter bilis or coinfected with Helicobacter hepaticus and Helicobacter rodentium and fed a lithogenic diet developed cholesterol gallstones at 80% prevalence by 8 weeks compared with approximately 10% in uninfected controls. Monoinfections with H hepaticus , Helicobacter cinaedi , and H rodentium gave a cholesterol gallstone prevalence of 40%, 30%, and 20%, respectively; the latter 2 groups did not differ significantly from uninfected animals. Neither infected nor uninfected mice fed a chow diet developed cholesterol gallstones. CONCLUSIONS: These findings, along with prior epidemiologic studies, suggest that Helicobacter spp play a major role in the pathophysiology of cholesterol gallstone formation in mice and perhaps humans.

Animals↗