Presence Of Helicobacter Research Articles

Alterações histológicas da pars esophagea de suínos e sua relação com Helicobacter spp.

A relação entre Helicobacter spp. e a presença de alterações histológicas na pars esophagea de suínos foi avaliada em 67 estômagos de animais em idade de abate. Para a identificação das helicobactérias, utilizou-se a técnica da PCR com primers específicos para o gênero Helicobacter. As alterações histológicas foram identificadas e classificadas como ulceração, erosão, degeneração epitelial, alongamento de papilas, hiperplasia, paraqueratose, intensidade do infiltrado inflamatório e aumento do número de folículos linfoides. As alterações mais frequentemente encontradas na pars esophagea foram a degeneração epitelial e o alongamento de papilas, observadas em 83,5% (n=56) das amostras analisadas. Em 77,5% (n=52) das amostras, observou-se paraqueratose e em 61,1% (n=41) hiperplasia epitelial. Quarenta e sete (70,1%) foram positivas na PCR para Helicobacter spp. Nessas amostras a erosão foi a lesão mais observada (40,2%), seguida de ulceração da mucosa (11,9%). Em 58,2% das amostras positivas na PCR, não foram observadas ulcerações de mucosa. Observou-se associação significativa (P=0,003) entre a presença de Helicobacter spp. e a degeneração epitelial da pars esophagea de suínos em idade de abate.

Assessment of Chronic Gastritis in Pet Dogs and its Relation with Helicobacter-Like Organisms

The aim of this study was to evaluate the prevalence of chronic gastritis in pet dogs, to determine the histopathologic changes of gastric mucosa and, to determine its relationship with canine gastric Helicobacter infection. Sixty percent (n = 18), 27% (n = 8) and 13% (n = 4) of the examined stomachs showed normal, congested and erosive gastric mucosa respectively. Histopathologic examination was confirmed the presence of chronic gastritis in 40% of dogs (n = 12). Lymphocytic-plasmacytic gastritis was the most common type of chronic gastritis. Gastric Helicobacter was detected in cytological examination of 26 out of 30 dogs (86.6%) but in the PCR analysis, 93% of gastric samples were positive for GHLO. There was no significant relation between the presence of Helicobacters and chronic gastritis (p>0.05). Follicular gastritis was detected in 12 cases (40%) and there was also no significant correlation between its presence and GHLO's infection (p>0.05). In conclusion, chronic gastritis can be considered as a prevalent disease especially in dogs. Nutritional and environmental factors as well as individual immune response may have role in induction of chronic gastritis, but the clinical significance of these histopathologic changes should be evaluated.

13C-Harnstoff-Atemtest als nicht-invasive Methode zum Nachweis von Helicobacter (Campylobacter) pylori

The 13C-urea breath test was used for diagnosing noninvasively the possible presence of Helicobacter (formerly called Campylobacter) pylori in 20 patients with dyspepsia (ten men and ten women, mean age 40.2 [24-74] years). H. pylori was cultured from 14 patients, while in six the culture was negative. The proportion of 13C in expired air was measured by isotope mass-spectrometer and expressed as Delta (basal value about 20%). A dose of 2.5 mg urea per kg body-weight (BW) was ingested after a standard meal. The test was repeated with 1.75 and 1.0 mg/kg BW in five subjects. Delta had increased significantly after 30 min in all H. pylori-positive patients (P less than 0.001). The maximal value after 90 min ranged from 38 to 114%; in the H. pylori-negative patients it was 24%. After 1.75 and 1.0 mg/kg urea the maximal value after 90 min was 39-52% and 30-52%, respectively. Using a dose of 2.5 or 1.75 mg/kg BW tagged urea one can reliably distinguish between presence and absence of H. pylori. It is sufficient to test a basal and a 90-min expired-air sample.

A critical evaluation of the evidence on a causal relationship betweenHelicobacter pyloriand otitis media with effusion

There is growing interest in the presence of Helicobacter pylori in the upper aerodigestive tract, and in the middle ear in patients with otitis media with effusion. Some studies have reported detecting H pylori in the middle ear, although reports to the contrary exist. In this study, we critically evaluate the evidence for the theory that H pylori in the middle ear plays a role in otitis media with effusion. We undertook a systematic review of all available studies investigating the presence of H pylori in the middle ear of patients with otitis media with effusion. The current literature was critically analysed using the key words and phrases 'Helicobacter pylori' 'otitis media with effusion', 'serous otitis media', 'glue ear' and 'middle ear'. Six original research papers were identified, studying a total of 203 patients and 27 controls; two of these papers were randomised, controlled studies and four were prospective, cohort studies. At present, there is poor evidence for the existence of H pylori-associated otitis media with effusion. Further research in the field is needed in order to delineate the presence of H pylori and its role in the pathogenesis of otitis media with effusion.

Prevalência de helicobactérias e alterações na mucosa gástrica de cães saudáveis

Prevalence, distribution and density of gastric helicobacter colonization were determined in 50 healthy dogs, characterizing the macroscopic and microcospic aspects of their mucosa. Helicobacter prevalence was 96%, with greater distribution in the gastric fundus and body. Although the presence of macroscopic alterations was high (58%), it was characterized as mild due to the predominance of less severe ones (65.5%). High prevalence of mostly monoclear cell infriltate (64.7%) was noted. Association between the presence of helicobacter and macro and microscopic alterations was not observed.

Low prevalence of Helicobacteraceae in gall-stone disease and gall-bladder carcinoma in the German population

Colonisation of the hepatobiliary system with bile-resistant Helicobacter spp. has been proposed as a novel risk-factor in the pathogenesis of gall-bladder carcinoma (GBC). There are reports that biliary Helicobacter colonisation is frequent in countries with a high incidence of gall-bladder carcinoma. However, the prevalence of Helicobacteraceae in the gall-bladders of patients with GBC in Germany, a region with a low incidence of GBC, is unknown. Therefore, gall-bladder tissue from 99 patients who had undergone cholecystectomy was tested, including 57 cases of gall-stone disease (GSD), 20 cases of GBC, and 22 control patients. The presence of Helicobacter spp. was investigated by culture, immunohistochemistry and a group-specific PCR targeting the 16S rRNA gene of all currently known Helicobacteraceae. Of the 99 cases investigated, only one patient with GSD was PCR-positive for Helicobacteraceae. For this individual, sequence analysis of the 16S rRNA gene showed that it had homology closest to the 16S rRNA sequence of Helicobacter ganmani. Helicobacteraceae were not detected by culture or immunohistochemistry. The low prevalence of Helicobacteraceae in the gall-bladders investigated suggests that Helicobacteraceae do not play a predominant role in the pathogenesis of GSD and GBC in the German population. The low prevalence could be a possible explanation for a relatively low incidence of GBC in the German population, despite the fact that GSD, the major risk-factor for GBC, is highly prevalent.

Detection of Helicobacter candidatus suis by pcr in oesophagogastric ulcers of swine in Italy

The aim of this study was to evaluate by PCR the presence of Helicobacter spp. in gastric mucus from the fundic region of the stomach and to investigate its role in oesophagogastric ulcers in swine bred and regularly slaughtered in Piedmont (Northern Italy). Stomachs from 595 regularly slaughtered swine were subjected to gross pathological examination in order to evaluate the presence of gastric ulcers (revealed in 75 cases, 12.6%). Histopathological examination was performed to better characterise erosions and ulcers. DNA extracted from gastric mucus collected from all the ulcer-affected and from 25 normal stomachs was submitted to PCR using Helicobacter spp. 16S rRNA gene target primers. Sixty-three percent (47/75) of the affected stomachs was positive as well as 24% (6/25) of the non-affected ones. Sequence analysis from 5 positive samples showed 99% homology with Helicobacter candidatus suis 16S ribosomal RNA gene.

Detection of Helicobacter spp. DNA in the oral cavity of dogs

The mode of acquisition of gastric Helicobacter spp. infection in dogs has not been determined. It is suspected that oral–oral and faecal–oral transmission may be involved. The present study sought to determine if Helicobacter spp. DNA is present in the oral cavity of healthy and vomiting dogs. Thirty-eight pet dogs (27 vomiting and 11 clinically healthy) were studied. The presence of Helicobacter spp. was determined by single and nested PCR evaluation of DNA extracted from saliva, dental plaque and gastric biopsy samples. Helicobacter spp. DNA was detected by nested PCR in 36 (94.7%) gastric biopsies, 17 (44.7%) dental plaque and 19 (50%) saliva samples out of the 38 dogs examined. Overall 27 (71.1%) dogs screened by nested PCR were found to harbour Helicobacter spp. DNA in the oral cavity (dental plaque and/or saliva). There was no significant difference in the prevalence of Helicobacter spp. DNA in the oral cavity of vomiting and healthy dogs, and the time from vomiting to oral sampling did not have significant impact. This study confirms the high prevalence of gastric Helicobacter spp. infection in dogs, and reveals that Helicobacter spp. DNA is detectable in the oral cavity of over 70% of dogs. These findings support the possibility of oral–oral transmission between dogs and that the canine oral cavity may act as source of non- pylori Helicobacter spp. infection for humans.

Helicobacter infection in hepatocellular carcinoma tissue

To investigate whether Helicobacter species (Helicobacter spp.) could be detected in hepatocellular carcinoma (HCC) tissue. 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. 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. Helicobacter infection exists in liver tissues of HCC patients. Helicobacter spp. infection is related with HCC, which needs further research.

EFFICACY AND LONG-TERM OUTCOME OF GASTRITIS THERAPY IN CHEETAHS (ACINONYX JUBATUS)

A prospective clinical trial evaluating efficacy and long-term outcome of treatments for lymphoplasmacytic gastritis in cheetahs (Acinonyx jubatus) was conducted. The study evaluated efficacy of 11 different antibiotic and antiinflammatory treatment protocols in 32 cheetahs (19 male, 13 female) for reducing gastric inflammation and Helicobacter colonization and monitored the course of disease through histologic grading of gastric biopsies. All cheetahs were biopsied up to I wk before treatment and then rebiopsied within 1 mo after treatment. Most animals were reassigned to a second treatment regimen within 6 mo. Each animal received from one to three treatments during the study period. After the trial, gastric biopsies were obtained from each cheetah annually until death or transfer from the facility to assess disease progression. The trial and follow-up period spanned 10 yr. At onset of the trial, all 32 cheetahs had some degree of gastritis, and 26 cheetahs (81%) were colonized with Helicobacter. Inflammatory lesions worsened regardless of treatment or the presence of Helicobacter. No treatment had a significant effect on inflammatory changes except the lansoprazole/clarithromycin/amoxicillin treatment group, which produced a short-term decrease in inflammation when compared to controls. Prednisone had no effect on gastric inflammation. Overall, 65% of colonized cheetahs were initially cleared of histologic evidence of Helicobacter by treatment, with short-term eradication occurring in 100% of the animals treated with omeprazole/clarithromycin/amoxicillin or tetracycline/metronidazole/Pepto-Bismol for 28 days. Long-term follow-up of treated animals in this study clearly demonstrated that these treatments had little effect on life-long progression of gastritis or on Helicobacter burden in individual cheetahs, although some treatments provided short-term reduction in gastritis and Helicobacter. These results provide evidence that Helicobacter alone is not the cause of gastritis in cheetahs and do not support the use of antibacterial treatments in cheetahs unless significant clinical signs (e.g., frequent vomiting/regurgitation, weight loss) are apparent.

Heme Oxygenase-1 Is Expressed in Carotid Atherosclerotic Plaques Infected by Helicobacter pylori and Is More Prevalent in Asymptomatic Subjects

It is not well established what are the features, if any, that distinguish symptomatic from asymptomatic carotid atherosclerotic plaques. Inducible heme oxygenase-1 (HO-1) is a component of cellular defense mechanisms against oxidative stress. We aimed to assess the presence of Helicobacter pylori (H pylori) and the expression of HO-1 in carotid atherosclerotic plaques of patients with and without prior neurologic symptoms attributable to the operated artery. We examined 25 symptomatic and 23 asymptomatic carotid atherosclerotic plaques removed during endarterectomy and 7 normal carotid arteries obtained at autopsy. We investigated the presence of H pylori DNA in the vessel wall and performed immunohistochemical detection of HO-1. H pylori DNA was present in 28 plaques and HO-1 was expressed in 30 plaques. HO-1 was found in 27 H pylori-positive specimens but in only 3 H pylori-negative specimens (P<0.001). All 7 normal carotid arteries were negative for both H pylori and HO-1. Although 82% of asymptomatic specimens were positive for H pylori and 87% for HO-1, only 36% of symptomatic specimens were positive for both H pylori and HO-1 (P<0.01). This study suggests a strong association between H pylori infection and expression of HO-1 in carotid atherosclerotic plaques. There was a substantial prevalence of these features in specimens obtained from asymptomatic subjects.

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.

Evaluation of seaFAST, a Rapid Fluorescent In Situ Hybridization Test, for Detection of Helicobacter pylori and Resistance to Clarithromycin in Paraffin-Embedded Biopsy Sections

A commercially available rapid fluorescent in situ hybridization (FISH) test, (seaFAST H. pylori Combi-Kit; SeaPro Theranostics International, Lelystad, The Netherlands) was used to simultaneously detect the presence of Helicobacter pylori and determine clarithromycin susceptibility in paraffin-embedded biopsy sections. The FISH method was found to be 97% sensitive, 94% specific for the detection of H. pylori and comparable to agar dilution for the detection of resistance to clarithromycin.

Quantitative Analysis of Inflammatory and Immune Responses in Dogs with Gastritis and Their Relationship to Helicobacter spp. Infection

The present study sought to quantitatively examine mucosal inflammatory and immune responses in dogs with gastritis and the relationship of these responses to infection with Helicobacter. Gastric biopsies from 30 dogs were evaluated for B- and T-lymphocytes, neutrophils, eosinophils, macrophages, and mast cells. Mucosal atrophy, fibrosis, cellularity, and severity of gastritis were graded qualitatively. Messenger-RNA (mRNA) for actin, interleukin-1beta (IL-1beta), IL-4, IL-8, and IL-10, transforming growth factor beta (TGF-beta), and interferon gamma (IFN-gamma) was quantified by polymerase chain reaction (PCR). The presence of Helicobacter spp. was determined by urease activity, histology, PCR, and enzyme-linked immunosorbent assay. mRNA for IL-1beta, IL-8, IL-10, TGF-beta, and IFN-gamma was detected in most dogs. IL-4 mRNA was detected in only 1 dog. Correlations were observed for IL-1beta versus IL-8 and IL-10; IL-8 versus IL-10, IFN-gamma, and TGF-beta; and IL-10 versus IFN-y. Mucosal pathology was related to cytokine mRNA expression (neutrophils to IL-8 and IFN-gamma, macrophages and lymphocytes to IFN-gamma, and fibrosis to IL-1beta). Gastritis was categorized as lymphoplasmacytic in all dogs, and its histologic severity correlated with atrophy, infiltration with lymphocytes and macrophages, and expression of IL-10 and IFN-gamma. Of the dogs examined, 76.7% were infected with Helicobacter spp. Infection was associated with increased expression of TGF-beta and fibrosis. Circulating anti-Helicobacter immunoglobulin G titers were higher in uninfected than infected dogs. We conclude that lymphoplasmacytic gastritis in dogs is characterized by concurrent activation of proinflammatory and immunomodulatory cytokines, with increased mRNA expression related to mucosal pathology. No significant associations between Helicobacter infection and proinflammatory cytokine expression, severity of gastritis, or differences in the pathogenicity of different Helicobacter spp. were found.

Fecal shedding of Helicobacter spp. by co-housed Australian sea lions ( Neophoca cinerea) and Australian fur seals ( Arctocephalus pusillus doriferus)

With the emergence of Helicobacter species as agents of gastrointestinal disease within a broad range of animal hosts, there is growing awareness of the need to identify such species and the potential role(s) they play within the intestine. Of interest in this study are captive seals and sea lions, where close proximity to one another may enhance the transmission of pathogens, in particular Helicobacter. The feces of several captive Australian sea lions and Australian fur seals were assessed for the occurrence of Helicobacter over 31 days. The presence of Helicobacter, detected by the polymerase chain reaction (PCR) varied over time and at times could not be detected. Helicobacter species were detected in five of the six animals examined of which two species were identified. This is the first report of Helicobacter species in captive seals and demonstrates the diversity and potential role(s) they may play in the gut of these animals.

The Prevalence of Erosive Esophagitis in Children: A Population-based Study

The Prevalence of Erosive Esophagitis in Children: A Populationbased Study Mark A. Gilger, Hashem B. El-Serag, Craig L. Dietrich Symptoms of gastroesophageal reflux disease (GERD) occur in 2-7% of children. The manifestations of GERD can be limited to symptoms (e.g. heartburn, regurgitation) or can be more complicated, such as erosive esophagitis (EE), esophageal strictures or Barrett’s esophagus. The prevalence of such GERD complications in children is unknown. PURPOSE: To determine the prevalence of endoscopic findings of EE in children.METHODS: All children aged 0 to 18 years who underwent EGD that was recorded in the Pediatric Endoscopic Database System Clinical Outcomes Research Initiative (PEDS-CORI) between 1999 and 2002 were included. Endoscopic reports that were incomplete, missing demographic features, indications for endoscopy or endoscopic findings were excluded. EE was defined either descriptively (erythema, erosion, ulcer) or by Los Angeles classification. Esophageal biopsy was not evaluated. RESULTS: 8038 children who underwent EGD fulfilled the inclusion and exclusion criteria. Of those, 1070 (13.3%) had EE. The mean age of children with children with EE was 12.6 (+/ 5.6) yrs vs. 10.0 (+/ 6.0) yrs in those without EE (p=<0.0001). There were 575 (53.7%) males with EE as compared with 3315 (46.7%) in those without EE (p=.0002). EE was found in 106 (9.9%) children aged 0-2 years, 73 (6.8%) children aged 3-5 years, 277 (25.9%) children aged 6-12 years, and 432 (40.4%) children aged 13-17 years. Hiatal hernia was found in 108 (10.1%) of children with EE, compared to 228 (3.2%) in those without EE (p=<0.0001). Mucosal abnormalities were identified in 390 (36.4%) of children with EE vs. 1327 (19.0%) of those without EE (p=<0.0001). The prevalence of Barrett’s esophagus, esophageal stricture, ulcer, prior surgery, nodules, foreign body/retained food and anatomical abnormalities were not significantly different between children with EE and those without. CONCLUSIONS: The prevalence of erosive esophagitis is slightly higher inmales and increases with age. In contrast to erosive esophagitis in adults, there were no significant variations according to race or ethnicity. Hiatal hernia is the only clinical observation that predicts the presence of EE. **470 The Presence of Helicobacter pylori in the Intestinal Mucosa is Closely Associated with Ulcerative Colitis Like Crohn’s Disease (UCLCD) Phenotype Dulciene M.M. Queiroz, Adriana G. Oliveira, Maria das Gracas P. Sanna, Andreia M.C. Rocha, Gifone A. Rocha Sr., Silvia B. Moura, Renato Dani, Maria de Lourdes A. Ferrari, Frederico P. Marinho, Liano S. Moreira, Lucia P.F. Castro Crohn’’s disease (CD) is a heterogeneous disorder with diverse clinical manifestations. Recently, fibrostenosing CD was associated with a serologic response to gut microbiota such as Pseudomonas fluorescens, ASCA and mutated allele of NOD2. We investigated whether the presence of Helicobacter in the intestinal mucosa was associated with specific disease phenotypes. We studied 117 patients: 74 controls and 43 with CD (22 with fibrostenosing, 16 with perforating and 12 UCLD). Fragments from the ileum and 6 different colon regions were obtained at colonoscopy. Helicobacter was investigated by culture, Helicobacter 16S rRNA, ureAnested PCR and characterized by 16S rRNA sequencing. Gastric HP infection was diagnosed by C-UBT and serology. Seven HP strains were isolated from the intestinal mucosa of 1 (2.2%) control and 6 (14.0%) CD patients (1with perforating and 5withUCLD) (p=0.02). SpecificHPDNAwas detected in the intestinal biopsies of 7 (9.5%) controls and 17 (39.5%) CD patients (p=0.0003).No otherHelicobacter species was identified.HPwasmore frequently isolated (47.1%v3.2%, p=0.004) or detected by PCR (58.3%v 22.6%, p=0.03) in the intestinal mucosa of patients with UCLD. If we considered only the group of gastric HP-positive patients, PCR was positive in 18.4% of the controls and in 100% of UCLD CD patients (p=0.00007). The positive results of culture (0.0% v 28.6%, p=0.009) and PCR (18.2% v 47.6%, p=0.04) were negatively associated with fibrostenosing disease. Positive culture was also inversely associated with ileal localization of CD (p=0.006). No association was seen between fistulating disease and positive culture (6.3% v 18.5%, p=0.4) and PCR (25.0%v 37.0%, p=0.4). Positive culture and PCRdid not associate with diarrhea in any subgroup. Gastric HP infection was similar in control (38-51.4%) and CD (21-48.7%) patients (p=1.0). However, the mean IgG titer against HP was lower (p=0.006) in CD patients (51.0U/ml) than in controls (239.7 U/ml). Furthermore, a significant difference was seen (p=0.04) between UCLD (103.8U/ml) and stenosing disease (24.5U/ml). We demonstrated associations between CD clinical phenotypes and the presence of viable HP or HP DNA in the intestinal mucosa that may indicate an abnormal higher number of HP in the intestinal mucosa or HP intestinal colonization in UCLD patients. Humoral immune response to HP infection was also influenced by CD phenotype, with a low reactivity to HP infection in stenosing disease phenotype.

Prevalence of Helicobacter pylori in Sri Lanka as Determined by PCR

Fifty-seven Sinhalese patients were investigated for the presence of Helicobacter pylori by PCR. A prevalence of 70.1%, with 47.5% positive for cagA, was demonstrated. The most common vacA allele was s1am1. There was no significant association between either the s1 allele or the cagA allele and severe gastroduodenal disease. There was an association between the s1 allele and the cagA locus.

Helicobacter Species Are Not Detectable by16S rDNA PCR in Bile from Dutch Patients with Common Bile Duct Stones

Background: Some Helicobacter species colonize the intestinal tract. To explore the possible relation between Helicobacter spp. and gallbladder disorders, we have investigated their presence in bile of patients with biliary obstruction and dilatation of the bile ducts. Methods: Bile was sampled from 31 Dutch patients with biliary obstruction identified by jaundice and dilatation of the bile ducts on ultrasound. Samples (n = 31) were obtained immediately following cannulation of the common bile duct (CBD) by endoscopic retrograde cholangiopancreatography (ERCP) (n = 29) or by peri-operative puncture of the galbladder (n = 2). DNA was isolated from bile by binding to diatoms. Helicobacter spp. were detected by a sensitive (detection limit 1 CFU per reaction tube) 16S rDNA PCR with genus-specific primers. Duplicate samples were spiked with Helicobacter pylori DNA and subjected to PCR in order to check for inhibition. Results: 28 patients had CBD stones (bile collected by ERCP (n = 26) or operatively (n = 2)), 2 had a pancreatic head tumor, and in 1 no abnormalities were found. In 1 of 21 amplifiable bile samples (10/31 inhibited) from Dutch patients with CBD stones, H. pylori 16S rDNA was found. Conclusion: Our data indicate that CBD stones in Dutch patients are not associated with the presence of Helicobacter spp. in bile.

The gastrins: their production and biological activities.

Gastric epithelial organization and function are controlled and maintained by a variety of endocrine and paracrine mediators. Peptides encoded by the gastrin gene are an important part of this system because targeted deletion of the gene, or of the gastrin-CCKB receptor gene, leads to decreased numbers of parietal cells and decreased gastric acid secretion. Recent studies indicate that the gastrin precursor, preprogastrin, gives rise to a variety of products, each with a distinctive spectrum of biological activity. The conversion of progastrin to smaller peptides is regulated by multiple mechanisms including prohormone phosphorylation and secretory vesicle pH. Progastrin itself stimulates colonic epithelial proliferation; biosynthetic intermediates (Gly-gastrins) stimulate colonic epithelial proliferation and gastric epithelial differentiation; and C-terminally amidated gastrins stimulate colonic proliferation, gastric epithelial proliferation and differentiation, and acid secretion. The effects of progastrin-derived peptides on gastric epithelial function are mediated in part by release of paracrine factors that include histamine, epidermal growth factor (EGF)-receptor ligands, and Reg. The importance of the appropriate regulation of this system is shown by the observation that prolonged moderate hypergastrinemia in transgenic mice leads to remodelling of the gastric epithelium, and in the presence of Helicobacter, to gastric cancer.

Gastritis and intestinal metaplasia in Syrian hamsters infected with Helicobacter aurati and two other microaerobes.

Chronic gastritis and intestinal metaplasia associated with naturally occurring colonization by Helicobacter aurati and two other microaerobic species were observed in Syrian hamsters. Thirty-five hamsters, between 7 and 12 months of age, were evaluated from two research and three commercial facilities. Microaerobic bacteria were cultured from the hamster stomachs. These bacteria included H. aurati, a fusiform, urease-positive species; a second novel helical, urease-negative Helicobacter sp.; as well as a smaller, urease-negative Campylobacter sp. Southern blot analysis detected Helicobacter spp. DNA in the gastric tissues of all 35 hamsters; 15 hamsters also had Campylobacter sp. DNA in their gastric tissues. When examined by light microscopy, argyrophilic bacteria consistent with H. aurati or the second Helicobacter sp. were present in antral sections of 12 out of the 15 hamsters where bacteria were seen, while 9 out of the 15 hamsters had bacteria resembling the Campylobacter sp. The presence of Helicobacter spp. but not the presence of Campylobacter sp. was significantly correlated to gastritis severity (P < 0.0001 for Helicobacter spp., P = 0.6025 for Campylobacter sp.) and intestinal metaplasia, as measured by numbers of goblet cells (P = 0.0239 for Helicobacter spp., P = 0.5525 for Campylobacter sp.). Severely affected hamsters also had Giardia sp. within their metaplastic gastric pits. Hamsters with naturally occurring helicobacter-associated gastritis provide a model for studying the development of intestinal metaplasia and gastric giardiasis in H. pylori-infected humans.