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Both Helicobacter pylori and Campylobacter jejuni are highly prevalent Gram-negative microaerophilic bacteria which are gastrointestinal pathogens of humans; H. pylori colonizes the gastroduodenal compartment and C. jejuni the intestinal mucosa. Although H. pylori causes chronic gastric infection leading to gastritis, peptic ulcers and eventually gastric cancer while C. jejuni causes acute infection inducing diarrhoeal disease, the endotoxin molecules of both bacterial species contrastingly contribute to their pathogenesis and the autoimmune sequelae each induces. Compared with enterobacterial endotoxin, that of H. pylori has significantly lower endotoxic and immuno-activities, the molecular basis for which is the underphosphorylation and underacylation of the lipid A component that interacts with immune receptors. This induction of low immunological responsiveness by endotoxin may aid the prolongation of H. pylori infection and therefore infection chronicity. On the other hand, this contrasts with acute infection-causing C. jejuni where overt inflammation contributes to pathology and diarrhoea production, and whose endotoxin is immunologically and endotoxically active. Futhermore, both H. pylori and C. jejuni exhibit molecular mimicry in the saccharide components of their endotoxins which can induce autoreactive antibodies; H. pylori expresses mimicry of Lewis and some ABO blood group antigens, C. jejuni mimicry of gangliosides. The former has been implicated in influencing the development of inflammation and gastric atrophy (a precursor of gastic cancer), the latter is central to the development of the neurological disorder Guillain-Barre syndrome. Both diseases raise important questions concerning infection-induced autoimmunity awaiting to be addressed.

Helicobacter pylori infection causes chronic active gastritis, ulcer disease, and gastric cancer. Current eradication regimens use a proton pump inhibitor (PPI) and two antibiotics. Triple therapy now has a success rate less than 80%, below the cutoff for efficacious eradication. Antibiotic resistance, inconsistent acid control by PPIs, and poor patient compliance contribute to the failure rate. H. pylori is a neutralophile that has developed special acid acclimation mechanisms to colonize its acidic gastric niche. Identifying the components of these mechanisms will provide novel bactericidal drug targets. Alternatively, better 24-hour acid control would increase the efficacy of antibiotics, leading to dual therapy with improved PPIs and amoxicillin. Studies of acid acclimation by H. pylori have identified several potential eradication targets including UreI, alpha-carbonic anhydrase, and a two-component system. Continuing improvement of PPIs has led to the development of at least three candidate drugs with improved 24-hour acid control.

Helicobacter pylori is an important human pathogen that causes chronic gastritis and is associated with the development of peptic ulcer disease and gastric malignancies. The oral cavity has been implicated as a potential H. pylori reservoir and may therefore be involved in the reinfection of the stomach, which can sometimes occur following treatment of an H. pylori infection. The objectives of this paper were (i) to determine the presence of H. pylori in the oral cavity and (ii) to examine the relationship between oral H. pylori and subsequent gastritis. Gastric biopsies, saliva samples and dental plaques were obtained from 78 dyspeptic adults. DNA was extracted and evaluated for the presence of H. pylori using polymerase chain reaction and Southern blotting methods. Persons with gastritis were frequently positive for H. pylori in their stomachs (p < 0.0001) and there was a statistically significant correlation between the presence of H. pylori in gastric biopsies and the oral cavity (p < 0.0001). Our results suggest a relationship between gastric infection and the presence of this bacterium in the oral cavity. Despite this, H. pylori were present in the oral cavity with variable distribution between saliva and dental plaques, suggesting the existence of a reservoir for the species and a potential association with gastric reinfection.

Objectives/Hypothesis: To determine if there is a relationship between Helicobacter pylori colonization in the pharynx mucous membrane and chronic nonspecific pharyngitis. Study Design: A prospective clinical study. Methods: Seventy patients with chronic pharyngitis and 20 healthy control subjects were examined with polymerase chain reaction (PCR) and culture for H. pylori colonization in the pharynx mucous membrane between March 2008 and October 2008. Patients with pharyngitis were seperated into two groups (35 patients in each) by using C-14 urea breath test, according to the presence of gastric H. pylori infection. Results: In the control group, none of the patients had H. pylori in the pharynx. In the chronic pharyngitis group, in 12 patients (34.3%) with gastric H. pylori infection and in seven patients (20%) without gastric infection, H. pylori colonization in pharynx mucosa was determined with the PCR method. In only two of chronic pharyngitis patients (5.8%), H. pylori infection was detected with culture. In the pharynx mucosa, the H. pylori infection rate was significantly higher in the chronic pharyngitis groups than in the control group (P = .002 between C-14 positive and control groups, P = .040 between C-14 negative and control groups). There was not a significant difference in H. pylori colonization in the pharynx of patients who had chronic pharyngitis with or without gastric ailments and H. pylori infection (P = .179). Conclusions: Chronic nonspecific pharyngitis without gastric H. pylori infection is significantly related to H. pylori colonization in the pharynx, and gastric involvement increases the rate of this spread. The gold standart for detection of H. pylori infection is the PCR method. Laryngoscope, 2009

BACKGROUND:Helicobacter pyloriis considered to be a pathogen responsible for gastritis and peptic ulcers, and a risk factor for gastric cancer. A periodontal pocket in the teeth of individuals with chronic periodontitis may function as a reservoir forH pylori.OBJECTIVE: The present study was undertaken to evaluate whether the presence ofH pyloriin the dental plaque of patients with and without periodontitis correlates with gastric involvement.METHODS: A total of 101 patients with dyspepsia were included in the present study. Subjects were divided into periodontitis and non-periodontitis groups. For the detection ofH pyloriin dental plaque, samples were collected from two teeth using a periodontal curette. Subgingival plaque was obtained by inserting two sterile paper points into periodontal pockets for 20 s. This was followed by an upper gastrointestinal endoscopy and antral biopsies.RESULTS: Sixty-five per cent of patients had dental plaque positive forH pyloriand more than 50% harboured the bacteria in their stomach. Periodontitis patients had a significantly higher percentage ofH pyloriin their dental plaque (79% versus 43%; PH pyloriin both dental plaque and the stomach.CONCLUSION: Patients with poor oral hygiene have a higher prevalence ofH pyloriin dental plaque and in the stomach. This finding suggests that the oral cavity may be a reservoir forH pylori,and potentially a source of transmission or reinfection.

At the turn of the twentieth century, gastric cancer was the leading cause of cancerrelated death in many Western countries but the incidence has steadily decreased over the past 70 years. Globally, gastric cancer is the second most common cause of cancer-related death and, as a result of population aging and growth, the predicted incidence for 2010 is 1.1 million with the majority of this health burden borne by economically lesser-developed countries. In this chapter, we hope to shed some light on the role of host genetic susceptibility in the pathogenesis of gastric cancer. In particular, we attempt to demonstrate how interactions among an infectious agent, host genetic makeup, and environmental factors could influence the pathogenesis of this cancer. The infectious agent in question is Helicobacter pylori, the world’s most common chronic bacterial infection and the malignancy is gastric cancer, second only to lung cancer in its global incidence and impact. We demonstrate how this gastric infection could be used as a paradigm for gene–environment interactions in human disease, one that could help unravel the unknowns of a multitude of other microbial-induced malignancies.

Since biliary enterogastric reflux is suggested to eradicate gastric infection with Helicobacter pylori (HP), we have investigated in a prospective randomized study the effect of partial gastrectomy with either Billroth II or Roux-en-Y anastomosis on infection with HP as assessed by the titers of IgG and IgA antibodies against HP in serum. These antibodies were measured by ELISA in serum of 22 patients before and at 10 days and 6, 15, and 24 months after either Billroth II (N = 11) or Roux-en-Y (N = 11) gastrectomy for peptic ulcer. All patients had HP demonstrated in their preoperative endoscopic gastric biopsies. The preoperative serum IgA antibodies against HP (anti-HP IgA) were increased in 20 of the 22 patients (range 0.21-1.69) while the IgG antibodies (anti-HP IgG) were increased in all 22 patients (range 0.38-1.31). Four of the Billroth II patients had clearance of HP from gastric biopsies accompanied by rapid and pronounced decrease of anti-HP IgA. In contrast, the patients with Roux-en-Y gastrectomy and the Billroth II patients with persistent HP infection had no change in anti-HP IgA after surgery. Anti-HP IgG showed variable results in the four patients without gastric HP infection and was not affected by gastrectomy in the patients with persistent HP infection. We concluded that serum anti-HP IgA, but not anti-HP IgG, is helpful in identifying those patients in whom HP is no longer demonstrable after Billroth II gastrectomy. Gastrectomy with Roux-en-Y anastomosis had no effect on gastric HP infection.

The possibility of using the rhesus monkey as a model for studying gastric function in the presence of infection with spiral bacteria was studied. Endoscopic evaluation of the gastric mucosa was performed under general anesthesia in 29 colony-bred rhesus monkeys, and gastric pinch biopsy specimens were obtained from each animal. On a separate day, gastric emptying and acid output were determined using a 99mTc dilution technique. Biopsy samples were fixed for light microscopy (HE (b) "G. hominis"-like, but not H. pylori-like organisms, invade and on occasion damage parietal cells while apparently causing hyperchlorhydria; and (c) the rhesus monkey appears to be a good model for the study of gastric infection with spiral bacteria.

Helicobacter pylori persistently colonizes the gastric mucosa of half the human population. It is one of the most genetically diverse bacterial organisms and subvariants are continuously emerging within an H. pylori population. In this study we characterized a number of single-colony isolates from H. pylori communities in various environmental settings, namely persistent human gastric infection, in vitro bacterial subcultures on agar medium, and experimental in vivo infection in mice. The lipopolysaccharide (LPS) O-antigen chain revealed considerable phenotypic diversity between individual cells in the studied bacterial communities, as demonstrated by size variable O-antigen chains and different levels of Lewis glycosylation. Absence of high-molecular-weight O-antigen chains was notable in a number of experimentally passaged isolates in vitro and in vivo. This phenotype was not evident in bacteria obtained from a human gastric biopsy, where all cells expressed high-molecular-weight O-antigen chains, which thus may be the preferred phenotype for H. pylori colonizing human gastric mucosa. Genotypic variability was monitored in the two genes encoding alpha 1,3-fucosyltransferases, futA and futB, that are involved in Lewis antigen expression. Genetic modifications that could be attributable to recombination events within and between the two genes were commonly detected and created a diversity, which together with phase variation, contributed to divergent LPS expression. Our data suggest that the surrounding environment imposes a selective pressure on H. pylori to express certain LPS phenotypes. Thus, the milieu in a host will select for bacterial variants with particular characteristics that facilitate adaptation and survival in the gastric mucosa of that individual, and will shape the bacterial community structure.

Background: Helicobacter pylori, the human pathogenic gram-negative microaerophilic bacterium, causes chronic gastric infection in more than half of the human population regardless of race. The infection of microbe is not yet controllable to pose a substantial public health impact and a growing social burden. The management of H. pylori infection primarily necessitates accurate and timely diagnosis at case level, on-demand supervision of pathologic progression, and reliable evaluation of the impact of pharmacologic interventions on the patients’ population. Methods: The characterization of H. pylori infection on gerbils model was performed by metabolic profiling, employing 1H NMR spectroscopy compounding multivariate pattern recognition strategies. In the same manner, urine samples were individually collected from 10 gerbils infected with H. pylori GS13, and from 10 uninfected control animals equally accessible to feed and water. Results: The resultant metabolic profiles indicate that H. pylori infection disturbs carbohydrate metabolism to elevate the levels of α- and β-glucose, and cis-aconitate (a TCA cycle intermediate). In addition to the energy metabolism alteration, the colonization of H. pylori in gerbil stomach generates a remarkable deviation of amino acid metabolism as indicated by depletion of taurine and arginine, and elevation of proline and glutamine in the animal urine. Moreover, the H. pylori infection modifies the gut microbiota as highlighted by a range of microbial-related metabolites such as indoxyl sulfate and hippurate. Conclusions: These findings demonstrate that the 1H NMR-based urine metabolic profiling is a promising technique capable of providing an accurate, noninvasive, and rapid diagnosis of H. pylori infection.

Background: Helicobacter pylori causes peptic ulcer disease and gastric cancer, and the oral cavity is likely to serve as a reservoir for this pathogen. We investigated the binding of H. pylori to the mucins covering the mucosal surfaces in the niches along the oral to gastric infection route and during gastric disease and modeled the outcome of these interactions. Materials and Methods: A panel of seven H. pylori strains with defined binding properties was used to identify binding to human mucins from saliva, gastric juice, cardia, corpus, and antrum of healthy stomachs and of stomachs affected by gastritis at pH 7.4 and 3.0 using a microtiter-based method. Results: H. pylori binding to mucins differed substantially with the anatomic site, mucin type, pH, gastritis status, and H. pylori strain all having effect on binding. Mucins from saliva and gastric juice displayed the most diverse binding patterns, involving four modes of H. pylori adhesion and the MUC5B, MUC7, and MUC5AC mucins as well as the salivary agglutinin. Binding occurred via the blood-group antigen-binding adhesin (BabA), the sialic acid-binding adhesin (SabA), a charge/low pH-dependent mechanism, and a novel saliva-binding adhesin. In the healthy gastric mucus layer only BabA and acid/charge affect binding to the mucins, whereas in gastritis, the BabA/Le(b)-dependent binding to MUC5AC remained, and SabA and low pH binding increased. Conclusions: The four H. pylori adhesion modes binding to mucins are likely to play different roles during colonization of the oral to gastric niches and during long-term infection. (Less)

Objetivo: La infección gástrica por Helicobacter pylori (HP) es considerada como un factor de riesgo importante en la patología arterial oclusiva. Actualmente se piensa que la coriorretinopatía serosa central (CSC) es una enfermedad por oclusión multifocal en la coriocapilar. El objeto de este estudio es valorar una posible relación patogénica entre la infección gástrica por HP y la CSC. Material y método: Se estudió un grupo de 16 pacientes con CSC y 20 controles. El estudio de la infección por HP se realizó con el test respiratorio de la urea-13C (TRU). El diagnóstico clínico de CSC se confirmó con biomicroscopía posterior y angiografía fluoresceínica. Resultados: De los 16 pacientes CSC, 11 (68,75%) fueron varones y 5 (31,25%) mujeres con una edad media de 46,3 años. La infección por HP fue positiva en 11 pacientes (68,75%) y negativa en 5 (31,25%). Los hombres fueron HP positivo (HP+) en el 72,7% de los casos frente a las mujeres que fueron HP+ en el 60%. La diferencia en prevalencia de HP entre el grupo-CSC (68,75%) y el grupo-control (30%) fue significativa (p< 0,05). Los pacientes HP+ tenían más dolores gástricos que los pacientes HP negativo (HP-) (72,73% vs 20%). Conclusiones: Estos resultados indican una posible asociación estadística entre la infección gástrica por Helicobacter pylori y la coriorretinopatía serosa central, pudiendo considerar la infección por HP como un posible factor de riesgo en los pacientes CSC. Objective: Helicobacter pylori (HP) gastric infection has been implicated as an important factor in occlusive arterial pathology. Nowadays, it is suspected that central serous chorioretinopathy (CSC) is due to a multifocal vascular occlusive disease of the choriocapillaris. The aim of this study was to determine the relation between gastric HP infection and CSC. Materials and methods: We evaluated a group of 16 patients with CSC and 20 controls. HP infection was assessed by the 13C-urea breath test (UBT). Clinical CSC diagnosis was confirmed by fundus biomicroscopy and fluorescein angiography. Results: Out of 16 patients with CSC, 11 (68.75%) were males and 5 (31.25%) females, with a mean age of 46.3 years. HP infection was positive in 11 patients (68.75%) and negative in 5 (31.25%). Men were HP-positive (HP+) in 72.7% of cases, compared to women who were HP+ in 60% of cases. The difference in prevalence of HP between the CSC-group (68.75%) and the control-group (30%) was found to be statistically significant (p< 0.05). HP+ patients had more gastric pain than HP negative (HP-) patients (72.73% vs 20%). Conclusions: These results indicate a possible statistical association between Helicobacter pylori gastric infection and CSC. HP should thus be considered a risk factor in CSC patients.

Isolation of a spiral-shaped bacterium closely related to Helicobacter pylori from the cat stomach made it possible to investigate new small animal models of gastric infection. Pure cultures of this bacterium, provisionally named "Helicobacter felis," were fed to germ-free mice. The organism colonized the stomach in large numbers in mucus and deep in the gastric pits and showed the same gastric trophism found with H. pylori. Significant histopathology was seen in all H. felis-infected mice. At 2 weeks postinfection, an acute inflammatory response was seen composed primarily of eosinophils and neutrophils. At 3 weeks, the polymorphonuclear response was more pronounced with large numbers of neutrophils in some areas forming small microabscesses. Lymphocytes also increased in number. By 8 weeks, several relatively large lymphoid nodules were present in the submucosa. Multiple small microabscesses were still present in the pyloric mucosa. This is the first animal model of bacterial gastritis to be described that shows progression from acute inflammation to persistent acute on chronic inflammation (active chronic) as is seen in human infection with H. pylori.

To evaluate the accuracy of IgG and IgA serological tests in establishing a diagnosis of Helicobacter (Campylobacter) pylori gastric infection, 60 children presenting with chronic abdominal pain were prospectively studied. Endoscopic antral biopsies were obtained and analyzed for the presence of H. pylori using three standard methods: culture and identification of bacterial isolates, microscopic examination for morphologically characteristic bacteria, and urease production by the biopsy specimen. Concomitantly obtained serum samples were analyzed for the presence of IgG and IgA antibodies against H. pylori surface antigens using enzyme-linked immunosorbent assay (ELISA). Thirty-four of 60 (56.6%) had histological evidence of chronic active gastritis, eight of whom (13.3%) also had evidence of H. pylori infection by at least one criteria. Six of the eight infected patients had H. pylori demonstrated by all three methods. Of the eight infected patients, seven had IgG antibodies against H. pylori (sensitivity of 87%) and six had IgA antibodies (sensitivity of 75%). Among the six patients who had H. pylori infection confirmed by all three methods, all had IgG antibodies (sensitivity of 100%). In the patients without evidence of H. pylori infection, the IgG ELISA had a specificity of 96% (50/52), and the IgA ELISA had a specificity of 100% (52/52). Our data suggest that serological testing for the presence of antibodies against H. pylori may be a useful diagnostic tool in screening children with chronic abdominal pain for the presence of gastric infection with H. pylori.

Establishment of infection with Helicobacter pylori and gastritis in nonhuman species is currently only successful in gnotobiotic piglets. This study was designed to determine whether H. pylori will colonize the gastrointestinal tract of gnotobiotic dogs. Gnotobiotic beagle pups were derived by standard methods. Group A (five dogs) was orally challenged with 3 x 10(8) H. pylori at 7 days of age. Group B (two dogs) received only peptone water but was contact-exposed beginning on day 23 postinfection (p.i.). Necropsy was performed on dogs on day 30 p.i. H. pylori colonized the stomach of all dogs (groups A and B). Urease map analysis correlated with the microbiologic findings and indicated that the density of colonization was less than that observed in human tissue. Organisms were also recovered from the pharynx, esophagus, duodenum, and rectum of 1, 2, 2, and 1 dog, respectively. All group A and one group B dog developed serum immunoglobulin G specific for H. pylori by day 30 p.i. Gross lesions were restricted to the stomach and consisted of small (less than 1 mm) lymphoid follicles. Microscopically, there were focal to diffuse lymphoplasmacytic infiltrates with follicle formation and mild to moderate infiltration of neutrophils and eosinophils in the gastric lamina propria. With the Warthin-Starry silver stain, organisms were seen on the surface of the gastric epithelial cells, beneath the mucus layer. We conclude that H. pylori colonizes the stomachs of gnotobiotic dogs for at least 1 month and the lesions resemble those seen in humans. H. pylori is transmissible by contact from infected to noninfected dogs.

Spasmolytic polypeptide (TFF2)-expressing metaplasia (SPEM) is observed in mucosa adjacent to human gastric cancer and in fundic glands showing oxyntic atrophy in Helicobacter felis-infected mice. Mongolian gerbils infected with Helicobacter pylori (Hp) develop goblet cell intestinal metaplasia and adenocarcinoma, but the presence of SPEM has not been studied in gerbils. We therefore have sought to examine the development of metaplastic mucosal changes in Hp-infected Mongolian gerbils. Mongolian gerbils were assigned to either uninfected controls or infected with Hp at 17 weeks of age. The animals were killed at 17, 20, 26, 31, 41 and 56 weeks of age. Stomach sections were stained using antibodies for TFF2, intrinsic factor, H/K-ATPase, BrdU and MUC2. Dual immunofluorescence staining for TFF2 with intrinsic factor and for TFF2 with MUC2 was performed. In uninfected animals, no SPEM or intestinal metaplasia was observed. Infected gerbils developed SPEM initially in the intermediate zone along the lesser curvature and subsequently spread out towards the greater curvature. In the earlier stages of infection, SPEM glands demonstrated TFF2 and intrinsic factor double staining cells. However, after 35 weeks of infection, the number of double staining SPEM cells decreased. While early in infection SPEM organized in straight glands, in the later stages of infections, SPEM glands became distorted or dilated along with the development of gastritis cystica profunda that was TFF2 positive. Goblet cell intestinal metaplasia developed only late in the infection. Dual staining for TFF2 and MUC2 showed glands containing both SPEM- and MUC2-positive goblet cell intestinal metaplasia. SPEM develops early in Hp infection in Mongolian gerbils, and alterations in gland morphology arise from SPEM glands during the course of gastric infection with goblet cell intestinal metaplasia developing subsequent to SPEM.

Objective To evaluate whether some duodenal ulcers (DU) classified as idiopathic according to standard criteria may be causally related to isolated duodenal colonization by H. pylori. Methods We studied consecutive ambulatory patients undergoing upper gastrointestinal endoscopy in a secondary care setting. Gastric and duodenal biopsies for diagnosing H. pylori infection were taken from all patients. Independently from the findings of duodenal biopsies, DU patients without gastric infection were classified as having idiopathic ulcers, and underwent urea C13 breath test and subsequent eradication therapy. Endoscopy was repeated 6 months after eradication treatment. Results Among 608 DU patients, 42 (6.9%) were classified as idiopathic: 24 (3.9%) were free from gastric and duodenal infection (group A) and 18 (3.0%) (group B) had isolated duodenal colonization. Urea C13 breath test was positive in one (4.2%) group A patient and in 3 (16.7%) group B patients. After eradication therapy, DU were detected in 14 out of 20 group A patients (70%) (four patients did not perform control endoscopy) and in 2 group B patients (11.1%): OR 18.66, 95% CI 3.23-107.82, P= 0.002. The difference was still detectable after multivariate analysis taking into account possible confounding factors: OR 15.79, 95% CI 2.48-100.53, P= 0.001. Conclusions Isolated duodenal colonization by H. pylori is detectable in a substantial proportion of patients with so-called idiopathic DU, and eradication therapy is effective in these patients.

It is known that patients infected with H pylori can spontaneously become free from infection, and that the reverse change can occur. The time-scale of these conversions is expressed as percentages per year. Since they have been investigated in terms of serology, the changes are called sero-reversion and sero-conversion respectively. Using serological evidence to investigate these phenomena is open to the criticisms that positive serology can be present in the absence of all other evidence of infection, and that a time-lag of 6-12 mo or longer can occur between eradication of the infection and sero-reversion. Investigations using direct evidence of current infection are sparse. The few that exist suggest that some individuals can seroconvert or sero-revert within six to twelve weeks. If these findings are confirmed, it means that some patients have an ability that is variable in time to resist, or spontaneously recover from, H pylori infection. Evidence suggests that the deciding factor of susceptibility is the level of gastric secretion of acid.

Gastric infection with the gram-negative bacterial pathogen Helicobacter pylori is widespread (approximately 50% of the human population is affected) and is associated with the induction of specific gastroduodenal disease. Although extensive studies in the H. pylori mouse model have demonstrated the feasibility of both therapeutic and prophylactic immunisations, the mechanism of vaccine-induced protection is still poorly understood. We report here on novel strategies to optimise the generation of H. pylori ghosts as vaccine candidates and highlight the need to concentrate on alternative animal models and the use of fully virulent H. pylori type I strains for vaccination. An effective vaccine strategy against H. pylori has the potential to significantly improve population health worldwide.

Helicobacter pylori from patients with different diseases, including so-called autoimmune thyroiditis, chronic tonsillitis and tonsillar cancer, was isolated and cultured. It was identified according to the genotype using labeled hybridization probes complementary to six sequences of cagA and vacA genes. Different types of strains were found in isolates from gastrointestinal tract and patients suffering from thy- roiditis. Six out of seven genotyped isolates from patients in our Department of Otorhinolaryngology and Head and Neck Surgery exhibited the same genotype, differing from isolates obtained from other patients; the 7th isolate originated from a patient who had undergone surgery for deviatio septi nasi, at the same time suffering from autoimmune thyroiditis, having confirmed gastric infection by H. pylori from biopsy. This data made it possible to formulate the hypothesis on probable association of specific H. pylori genotype with chronic tonsillitis and tonsillar cancer. We assessed commercial transport media and improved nucleic acid isolation techniques and the RT-PCR-based tests, which allowed us to skip a culture step and to test directly the patients' samples; however, for full confirmation of our hypothesis and explanation of possible mecha- nisms of the contribution of Helicobacter sp. to the pathogenesis of the disease further data are to be col- lected and evaluated.

Helicobacter pyloriis a gastric-dwelling pathogen responsible, with acid secretion, for peptic ulcer and a 20-fold increase in the risk of gastric cancer. Several transcriptomes have been described after short-term exposure to acidityin vitro, but there are no data identifying the effects of chronic gastric exposure on bacterial gene expression. Comparison of thein vivoto thein vitrotranscriptome at pH 7.4 identified several groups of genes of known function that increased expression >2-fold, and three of these respond both to acidityin vitroand to gastric infection. Almost all known acid acclimation genes are highly up-regulated. These includeureA,ureB, androcFand the pH-gated urea channel,ureI. There is also up-regulation of two groups of motility and chemotaxis genes and for pathogenicity island genes, especiallycagA, a predictor for pathogenicity. Most of these genes interact withHP0166, the response element of the pH-sensing two-component histidine kinase,HP0165/HP0166, ArsRS. Based on the pH profile of survival ofureIdeletion mutantsin vitroand their inability to survive in gastric acidity, the habitat of the organism at the gastric surface is acidic with a pH ≤ 4.0. Hence, the pH of the habitat ofH. pylorion the surface of the stomach largely determines the regulation of these specific groups of genes.

BACKGROUND AND AIMS: Helicobacter pylori (H. pylori) is an important pathogen in gastritis, peptic ulcer and possibly gastric cancer, but several questions remain unanswered. Particularly how the organism is transmitted and what is the relationship between oral presence of H. pylori and the gastric infection. Accordingly, we aimed to characterize the H. pylori in oral cavity and to evaluate its relationship to gastric H. pylori infection. MATERIALS AND METHODS: Out of total 100 screened for H. pylori infection female subjects (40 to 85 y), 49 patients (pts), who had positive C-urea breath test (UBT) and dyspeptic symptoms, agreed for 1 week regimen of triple anti-H. pylori therapy. The presence of H. pylori in oral cavity was assessed using bacterial culture from saliva and gingival pockets. Gastric H. pylori infection was estimated using capsulated C-urea breath test and plasma anti-H. pylori IgG and saliva IgA antibodies. In addition, plasma gastrin, ghrelin, and pepsinogen I were measured by radioimmunoassay. In selected patients, gastroscopy was additionally performed and gastric biopsy samples were taken for H. pylori random amplification of polymorphic DNA genetic profiling. RESULTS: The triple therapy resulted in gastric H. pylori eradication in 79% pts, along with significant decrease of plasma gastrin combined with an increase in plasma ghrelin and pepsinogen I (PgI) levels and a marked alleviation of dyspeptic symptoms. In contrast to gastric effects, the eradication therapy failed to cause any changes in the presence of H. pylori in oral cavity. Moreover no relationship was observed between the presence of H. pylori in oral cavity and the gastric H. pylori eradication. In line with these findings, no relationship between gastric and oral H. pylori was found using genetic profiling by random amplification of polymorphic DNA. CONCLUSIONS: H. pylori was detected both in the oral cavity and the stomach but oral H. pylori had no relation to gastric H. pylori and remained unaffected by eradication of gastric H. pylori.

Background This clinical and microbiological study investigated whether Helicobacter pylori colonizes the mouth en route to the pyloric antrum. It has been suggested that oral colonies are a source of reinfection after eradication of gastric infection. Methods Some 208 patients attending for routine diagnostic endoscopy for dyspepsia were recruited. Before endoscopy, samples were collected of saliva, supragingival and infragingival plaque, and swabs were taken from the tongue, mouth and pharynx. At endoscopy, gastric antral biopsies were taken for the rapid urease test, culture and histological examination. Gastric and duodenal juice samples were aspirated. Restriction nuclease digestion with HaeIII was employed on all specimens from patients in whom there was evidence of the organism in the mouth. Results H. pylori was observed in dental plaque in only 15 patients, all from the 116 who had evidence of the organism in the stomach. Restriction endonuclease digestion demonstrated that in 13 of the 15 patients the strains were identical in mouth and stomach. Conclusion Oral colonization is a rare event, but does occur. Its rarity suggests that it is not an important factor in reinfection.

Helicobacter pylori infection of the human stomach causes chronic gastritis that can lead to gastric cancer. Because activated lymphocytes persist in the gastric mucosa, and because a high multiplicity of infection (MOI) of H. pylori is needed to induce apoptosis in vitro, we speculated that resistance of lymphocytes to apoptosis is an important feature of the immune response to H. pylori. Freshly isolated mouse splenocytes underwent substantial spontaneous apoptosis and displayed a biphasic response to H. pylori, in which low MOI (1-10) markedly inhibited apoptosis, whereas high MOI (≥75) potentiated apoptosis. Low MOI reduced mitochondrial membrane depolarization, caspase-3 and caspase-9 activation, and cytochrome c release and increased Bcl-2 levels. Low MOI also induced cellular proliferation. When cells were subjected to fluorescence-activated cell sorting after coculture with H. pylori, CD19+ B cells were found to be protected from apoptosis and undergoing proliferation at low MOI, whereas CD3+ T cells did not exhibit this pattern. The protective effect of low MOI on apoptosis persisted even when B cells were isolated before activation. Immunophenotyping showed that all B-cell subsets examined were protected from apoptosis at low MOI. Additionally, gastric infection with H. pylori resulted in protection of splenic B cells from spontaneous apoptosis. Our results suggest that the low levels of H. pylori infection that occur in vivo are associated with B-cell survival and proliferation, consistent with their potential to evolve into mucosa-associated lymphoid tissue lymphoma. (Cancer Res 2006; 66(13): 6834-42)

H. heilmannii belongs to the Helicobacter family and is found in a small number of gastric biopsies. This bacterium is generally found in primates, cats, pigs, and carnivorous mammals. About 0.5% to 6% of human gastric infections have been attributed to H. heilmannii. The bacterium usually induces mild chronic gastritis but may be associated with peptic ulceration, and rare cases were reported in association with gastric carcinoma and mucosa-associated lymphoid tissue lymphoma. We report a case of H. heilmannii chronic gastritis in a 44-year-old man with a history of chronic heartburn, found to have erythema and granularity in the antrum. Antral biopsy showed mild chronic gastritis with prominent lymphoid aggregates, and rare long, thin, spiral bacilli were present adjacent to the surface epithelium. The long tightly coiled morphology suggestive of H. heilmannii was obvious at 1000 x magnification. The lack of information in the literature regarding cross-reactivity of H. heilmannii to commercially available antibodies used for immunohistochemical detection of H. pylori prompted us to evaluate whether commercially available polyclonal anti-H. pylori antibodies show cross-reactivity between the two organisms. The H. pylori immunostain highlighted H. heilmannii organisms and their characteristic morphology, confirming cross-reactivity with the anti-H. pylori polyclonal antibody. This case illustrates the potential contribution of commercially available polyclonal antibodies against H. pylori to help confirm a diagnosis of H. heilmannii gastritis. The use of immunohistochemical stain to identify H. heilmannii may be useful in cases with a paucity of organisms, with suggestive but not diagnostic forms on routine hematoxylin and eosin stain.

Background. Helicobacter pylori is a curved microaerophilic Gram-negative bacterium considered as a risk factor for gastric cancer. The aim of this study was to find an association between burning sensations, acid taste, halitosis, and lingual hyperplasia with the effect of H. pylori on the mouth. Materials and Methods. A total of 124 subjects with different gastric diseases were studied: 46 patients with burning, halitosis and lingual dorsum hyperplasia and 78 patients with other diseases. Results. The detection of H. pylori in the oral cavity by histopathologic diagnosis and molecular biology was confirmed in 40/46 (87%) patients with burning, halitosis, and lingual hyperplasia, and in 2/78 (2.6%) subjects with other diseases. χ2: 91.26 (p

The earliest recorded history of autoimmune gastritis can be traced to 1849 in London, when Thomas Addison described "a very remarkable form of anemia" later called pernicious (fatal) anemia (PA). This was followed by the recognition of a gastric mucosal defect suspected to have a nutritional basis, the discovery of the megaloblast that characterized the anemia, the insufficiency of a dietary extrinsic factor characterized as vitamin B12 (cobalamin), and a gastric-secreted intrinsic factor. Treatment with vitamin B12 proved curative. The link between PA and gastritis and atrophy was first confirmed histologically after immediate fixation of the stomach postmortem and later, in the 1940s, by peroral tube biopsy. The causes of gastritis remained enigmatic until the era of autoimmunity, when autoantibodies were detected first to gastric intrinsic factor and then to gastric parietal cells. Hints of a dichotomy in pathogenesis of gastritis were crystallized by the description in 1973 of Type A (Autoimmune) and Type B (later, Bacterial) gastritis. Clarification was enhanced by identification in Type A gastritis of the autoantigen of the parietal cell antibody, by the alpha and beta subunits of gastric H+/K+ ATPase, and by the highly informative experimental murine model of postneonatal thymectomy autoimmune gastritis, and in Type B of the causative role of gastric infection with Helicobacter pylori (H. pylori). A denouement will require a full understanding of (1) the origin and pathogenetic contribution of antibody to intrinsic factor; (2) the connection, if any, between H. pylori infection and Type A autoimmune gastritis; and (3) the genetic contributions to gastritis, whether due to autoimmunity or to H. pylori infection.

Background and Aims Helicobacter pylori infections continue to be a major challenge to the field of gastroenterology. Gastric H. pylori infections is a critical cause of chronic atrophic gastritis and peptic ulcer disease and is one of the leading carcinogens that leads to stomach cancer and MALT lymphoma. Helicobacter pylori infection has been demonstrated to modulate the local inflammatory response in the gastric mucosa. In this study, we examine the role of chronic in vivo H. pylori infection in the modulation of inflam-mation controlled by Supressors of Cytokine Signalling (SOCS), a family of anti-inflammatory regulators that act on various cytokine pathways. Methods C57Bl6 mice were infected at 5 weeks of age with the mouse-adapted H. pylori strain SS1 via oral gavage × 3 inoculations. The mice were culled 20 weeks post-infection and the stomach tissue harvested post-mortem and snap frozen. Total RNA was extracted from these tissues and cDNA produced from the mRNA by reverse transcription. A semi-quantitative real time PCR study was conducted examining Socs1 and Cish relative gene expression in infected ( n = 10) and uninfected controls ( n = 10). Results Mice infected with H. pylori had a significantly increased gene expression of Socs1 ( p Cish gene expression was not signifi-cantly altered upon infection. Conclusions Helicobacter pylori may supress localised inflam-mation via increased expression of SOCS1 in a murine model of chronic infection.

Gastric infection with Helicobacter pylori is one of the most common chronic infections in humans, causing substantial morbidity and mortality. The diagnosis of H. pylori infection usually involves upper endoscopy with biopsy since the only noninvasive method of comparable accuracy, the [ 13 C]urea breath test, requires technical equipment that is not available in most gastroenterological units. Serological methods for detection of H. pylori infection have reached sufficient accuracy to be used as screening tests before endoscopy or for seroepidemiological surveys. In the present study we evaluated different interpretation criteria for use with immunoglobulin G immunoblotting for the diagnosis of H. pylori infection. We applied five different sets of interpretation criteria, four of which had been published previously, to the Western blot results of 294 patients with different gastrointestinal symptoms. Since it is known that less than 2% of patients who are infected with H. pylori fail to seroconvert, an optimally sensitive Western blotting system should be able to detect approximately 98% of active infections. When the different criteria were applied to our patient population, it became apparent that the abilities of the systems to detect active H. pylori infection were quite varied. The results for the sensitivity and specificity, according to the different applied criteria, ranged from 62.8 to 95.9% and from 85.7 to 100.0%, respectively. Positive predictive values and negative predictive values, according to the published criteria, ranged from 97.2 to 100.0% and from 37.7 to 82.4%, respectively. Recommendations for the optimal use of the different interpretation criteria are discussed.

The newly recognized murine pathogen Helicobacter hepaticus is known to colonize the ceca and colons of several strains of mice from a variety of commercial suppliers. Additionally, the organism persistently infects mice, causes a chronic hepatitis, and is linked to hepatic tumors in the A/JCr inbred mouse strain. For this reason, eradication of the organism from infected mouse colonies is desirable. Treatment modalities for eradication of H. hepaticus from the gastrointestinal system consisted of oral administration of various antibiotic combinations previously evaluated for eradication of experimental H. felis gastric infection in mice. A/JCr mice (8 to 10 weeks old) naturally infected with H. hepaticus were divided into six treatment groups of 10 animals each. Animals received monotherapy of amoxicillin, metronidazole, or tetracycline or triple therapy of amoxicillin-metronidazole-bismuth (AMB) or tetracycline-metronidazole-bismuth (TMB). All medications were administered by oral gavage three times daily for 2 weeks. One month after the final treatment, mice were euthanatized and livers, ceca, and colons were cultured for H. hepaticus. All untreated control animals had H. hepaticus isolated from the cecum and/or colon. H. hepaticus was not recovered from the livers, ceca, or colons of the AMB or TMB treatment groups. All animals receiving the various antibiotic monotherapies had H. hepaticus isolated from the cecum and colon. We conclude that at the doses and the route evaluated, AMB and TMB triple therapies are effective for eradication of H. hepaticus in 8- to 10-week old A/JCr mice.

The relation between Helicobacter pylori and gastroesophageal reflux disease is unclear. Recent reports have suggested a possible protective role for H. pylori, particularly in preventing the complications of gastroesophageal reflux disease (GERD). The purpose of this article is to present a brief overview of the recent literature regarding the role of H. pylori in the genesis of the complications of GERD, focusing on Barrett’s esophagus and esophageal adenocarcinoma. The prevalence of H. pylori infection in the population of the West is around 40% and is not different in cohorts of patients with GERD. When the infection induces pangastritis or corpus-predominant gastritis, there may be concomitant reduced gastric acid secretion. Eradication of the bacteria in this subgroup of patients may enhance gastric acid secretion and provoke reflux symptoms. H. pylori organisms do not colonize the specialized intestinal metaplasia characteristic of Barrett’s esophagus. H. pylori infection rates in gastric mucosa of patients with Barrett’s esophagus occur at a similar or slightly lower frequency than is found in controls. Gastric infection with cagA-positive strains of H. pylori appears to be uncommon in patients with Barrett’s esophagus. Furthermore, epidemiologic studies indicate that cagA-positive strains are protective against esophageal adenocarcinoma. Several investigators have proposed that the decreasing prevalence of H. pylori infection might be an important factor in the rising incidence of this tumor.

Background: Gastric infection with Helicobacter pylori is the major cause of chronic active gastritis and is associated with the pathogenesis of peptic ulcer and gastric carcinoma. Gastric mucosal damage involves both host and H pylori dependent factors, such as the presence of the cag pathogenicity island and allelic variations of the vacA and iceA genes. Aims: To evaluate the association of these virulence factors with the development of gastric malignancies, a retrospective study was performed on archived tissue routinely obtained for diagnostic histopathology. Methods: DNA was extracted from formalin fixed, paraffin wax embedded gastric tissue sections of 93 patients with chronic active gastritis (n = 39), adenocarcinoma (n = 28), or mucosa associated lymphoid tissue (MALT) lymphoma (n = 24). The extracted DNA was used to perform a polymerase chain reaction based, simultaneous analysis of the following: (1) cagA status, (2) allelic variation of the iceA genes (iceA1, iceA2), allelic variation of the signal peptide (s1a, s1b, s2) and the midregion (m1, m1a, m2) of the vacA gene. Results: The iceA1 gene showed a 3.6 fold and the vacA s1a variant a 4.2 fold higher prevalence in gastric adenocarcinoma than in gastritis. The combined presence of both the vacA s1a and iceA1 genes had a 5.6 fold higher frequency in adenocarcinoma. The vacA m2 allele was the predominant subtype in MALT lymphoma and the combination of the vacA m2 subtypes with the vacA s1 and the iceA1 variants occurred in MALT lymphoma nearly five times more often than in chronic active gastritis. Conclusions: Certain H pylori subtype combinations possess a differentiating and predictive value for the development of gastric adenocarcinoma and MALT lymphoma.

The link between Helicobacter pylori and gastric infection and malignancy has been firmly established since the discovery of this organism 20 years ago, and, in addition, there are now several studies implicating H. pylori infection as a risk factor for cardiac1–3 and other extraintestinal diseases. Furthermore, among the more than 20 Helicobacter species currently described, several have been linked to hepatobiliary and intestinal diseases. The human liver is normally sterile and has effective systems to escape bacterial pathogens. The biliary tree is likewise normally sterile but, when bile stones are present various microbes can be cultured from or detected in bile or the gallbladder wall4,5. Salmonella spp and Enterococcus spp can grow in the presence of bile, having been regularly isolated from chronic carriers and patients with cholecystitis, respectively6. Various conditions such as common bile duct or cystic duct obstruction, or infection can decrease the pH of bile which in turn could enhance the survival of H. pylori in a bile-rich environment7.

Novel anti-Helicobacter pylori antibiotics, pyloricidins A, A 1 , A 2 , B, C and D, were discovered in the culture broth of two bacilli strains. Pyloricidins selectively inhibited the growth of H. pylori. Pyloricidin B was efficacious in the treatment of gastric infection caused by H. pylori in Mongolian gerbils and may be promising for cure of H. pylori infection as a single agent.

Gastric infection with Helicobacter heilmannii (previously known as Gastrospirillum hominis ) is invariably linked with the presence of chronic gastritis and the risk of developing low-grade mucosa-associated lymphoid tissue lymphoma in humans. In contrast to Helicobacter pylori , various H. heilmannii species colonize the stomachs of domestic animals, which might be a reservoir for transmission to humans (zoonosis). To identify the number and prevalence of different H. heilmanni types in humans, we analyzed 89 gastric biopsy samples histologically identified as H. heilmannii positive by fluorescence in situ hybridization. Of these gastric specimens, 84 (94.4%) contained a single H. heilmannii type. In five samples, however, two different H. heilmannii types were detected. The most prevalent species in monoinfected samples is H. heilmannii type 1, found in 78.5% (66 of 84) of the specimens, followed by a novel H. heilmannii -like organism (HHLO), HHLO type 4, identified in 9.6% (8 of 84) of tissue sections. H. heilmannii type 2 and a further HHLO type not described before, type 3, were found in 8.3% (7 of 84) and 1.2% (1 of 84) of the monoinfected samples, respectively. Additionally, HHLO type 5 with a 16S ribosomal DNA sequence identical to that of Helicobacter salomonis was found with a prevalence of 2.4% (2 of 89). Thirteen of these biopsy samples were also investigated by a PCR approach developed for this study that allows a Helicobacter -specific amplification of a variable portion of the 16S rRNA gene and subsequent sequencing. In total, five different types of HHLOs could be identified within these samples. We conclude that humans can be infected by at least five different HHLO types, which presumably have their origin in animal species like dogs, cats, and pigs.

Mucosal candidosis is common in acquired immune deficiency syndrome (AIDS) patients, where there is extensive mucosal involvement, but rarely dissemination. To mimic this disease, SCID mice were inoculated orally with Candida albicans, which could be recovered from standardized tissue samples of the esophagus, stomach, small intestine and caecum of all mice. Treatment with fluconazole at 5 or 10 mg kg(-1) per day were equivalent to each other and efficacious in reducing the fungal burden from all four tissues compared with no treatment or lower doses of fluconazole (P0.01-0.001). Fluconazole at 5 or 10 mg kg(-1) reduced fungal burden in the stomach by about 200 or 580-fold, respectively, and by approximately 25-fold in the other tissues, with 80 or 100% of mice cleared of esophageal infection, and 40 or 80% cleared of infection in the small intestine, respectively; the same doses clearedor =20% of stomach infection and none of caecal infection. Treatment with recombinant human granulocyte colony-stimulating factor (G-CSF) up to 500 microg kg(-1) per day or 10(5) U of murine interferon-gamma (IFN-gamma) alone was ineffective, nor were combinations with a suboptimal dose fluconazole synergistic. Overall, fluconazole had dose-responsive efficacy, whereas neither G-CSF nor IFN-gamma alone or in combination with fluconazole improved efficacy. These studies demonstrate the utility of this model for examining antifungal efficacy in a situation that mimics clinical disease in AIDS patients.

The in vivo antibacterial activities of 7alpha-methoxy-cephems or 7alpha-methoxy-1-oxacephems and their demethoxy congeners after oral administration were compared in a mouse model of gastric infection with Helicobacter felis. The MICs of all four pairs of compounds with and without the 7alpha-methoxy substituent were within one two-fold dilution for H. felis and Helicobacter pylori, but the 7alpha-methoxy compounds were at least four-fold more active at bacterial eradication than their demethoxy congeners. Since these compounds are not absorbed after oral administration, they are likely to have gained direct access to the bacteria from the gastric cavity. Thus the 7alpha-methoxy substituent may enhance in vivo activity by promoting the gastric mucus permeability of the compounds or by allowing the compounds to remain longer in the gastric cavity.

Background: Helicobacter pylori has been involved in gastric epithelial cell damage and gastric gland loss or atrophy. Aims: to evaluate role of Helicobacter pylori infection in acute and chronic changes of chronic gastritis in a high gastric cancer-risk population. Material and methods: 200 patients with chronic gastritis were selected from pathological files of Temuco Hospital. A complete histopathological protocol was fulfilled considering the presence of infection by Helicobacter pylori-like-organism (HLO), acute and chronic inflammatory infiltrate, epithelial cell damage and epithelial cell regeneration. Results: 82% of patients showed infection by HLO. Moreover, this infection reached a frequency of 92.7% in gastric ulcer patients and 94.4% in duodenal ulcer patients. A statistically significant positive correlation was found between HLO infection and polymorphonuclear infiltrate, Iymphocytic infiltrate, mucus depletion and epithelial regenerative activity. There was not a statistical correlation between HLO infection and atrophy. Finally, 90% of patients with multifocal atrophic gastritis and 100% of patients with diffuse antral gastritis had HLO infection. Conclusions: HLO gastric infection frequently caused acute inflammatory changes in gastric mucosa with chronic gastritis. Sometimes these changes were severe, with marked polymorphonuclear migration throughout epithelium and severe epithelial cell damage. Recovery of these changes could be considered as a goal in Helicobacter pylori eradication therapy decision

Background. The goal of this study was to see whether Helicobacter pylori (H. pylori) in the oral cavity might adversely affect the outcome of eradication therapy for gastric H. pylori. Materials and Methods. Forty-seven patients (36 males, 11 females) with gastric H. pylori infection were enrolled in this study. Gastric H. pylori infection was confirmed by both immunohistological staining with anti-H. pylori antibody and bacterial culture of biopsy specimens. The therapeutic regimen consisted of 30 mg/day lansoprazole, 750 mg/day metronidazole, and 400 mg/day clarithromycin administered for 2 weeks. A fragment of the H. pylori urease gene was amplified by nested PCR for DNA extracted from saliva and dental plaque from the same patients. We examined the correlation between the gastric eradication success rate and the prevalence of H. pylori in the oral cavity as determined by PCR before and after the eradication therapy. Results. The eradication success rate was significantly lower in the oral H. pylori-positive cases (12/23, 52.1%) than in the negative cases (22/24, 91.6%) at 4 weeks after the therapy (p = .0028). Two years later, only 16 of the 23 (69.5%) oral H. pylori-positive cases were disease-free, as compared to 23 of the 24 (95.8%) oral H. pylori-negative cases (p = .018). Conclusions.H. pylori in the oral cavity affected the outcome of eradication therapy and was associated with a recurrence of gastric infection. We recommend that oral H. pylori should be examined by nested PCR and, if positive, should be considered a causal factor in refractory or recurrent cases.

Helicobacter pylori infection is mainly acquired in childhood and may predispose to peptic ulcer or gastric cancer later in life.1 Non-invasive diagnostic tools are particularly useful in children as screening tests and for epidemiological studies, but their accuracy has to be tested against that of invasive tests in symptomatic patients before they are used in any particular population. Of the non-invasive tests now available, serological testing is not accurate in young patients and the 13C urea breath test is expensive. In 1998 an enzyme linked immunoassay (ELISA) (Premier-Platinum-HpSA, Meridian Diagnostics, Cincinnati, OH, USA) was approved by the Food and Drug Administration for both diagnosis in adult symptomatic patients, and monitoring the response to treatment. It is now commercially available, but its correlation with gastric infection has not been assessed in children. We evaluated its diagnostic accuracy against invasive tests in children undergoing endoscopy for clinical evaluation, and we determined the cut off values for the paediatric population. View this table: Test performance calculated according to different reading techniques (at 450 …

Helicobacter pylori infects at least half of the world’s human population. Increasing evidence points to acquisition of the gastric infection during the childhood years1. Intrafamilial clustering suggests person-to-person transmission of the infection which could occur by the faecal-to-oral route, an oral-to-oral route, or via vomitus2,3. Recent reports of successful culture of viable bacteria from emesis provide additional support for the latter method of transmission4. However, precisely how this route of transmission would explain transfer of infection from infected parents to their uninfected young children remains enigmatic.

Infection of human stomach by Helicobacter pylori, a gram negative spiral bacterium first isolated in 1983 from a patient with chronic active gastritis (1), causes nearly all duodenal ulcers and most gastric ulcers and is associated with an increased risk of gastric adenocarcinoma (2). Current therapies for gastric infections include combination triple or quadruple therapy of antimicrobial and/or antiulcer agents for eradication of H. pylori infection (3). Development of the resistant strains and ecological niche (habitant) of the bacteria may cause relapse after the termination of the therapy. However, if effective, the high cost, difficulty of patient compliance and risk of selection for resistant strains make these therapeutic regimens impractical on a large scale, though effective on the laboratory trial stages. Studies of the pathogenesis of H. pylori have led to the identification of bacterial antigens and adherin proteins as candidates for inclusion as novel vaccines against these diseases (4-7). Both prophylactic and therapeutic vaccination have been demonstrated in animal models of H. pylori infection (8-10).

Chronic pancreatitis is a syndrome involving progressive inflammatory changes in the pancreas that result in permanent structural damage, and ultimately impairment of exocrine and endocrine function [1]. In the last 2 years we observed five patients referred for possible chronic pancreatitis based on moderately elevated levels of serum amylase and lipase and abnormal ultrasonographic imaging (Table 1). Family history of chronic pancreatitis (hereditary pancreatitis) was negative and none of the patients were receiving drugs known to cause pancreatic damage. Cessation of alcohol intake and small meals low in fat was the only treatment undertaken from the patients. All patients had active H. pylori infection, with a histological diagnosis of chronic active gastritis, without peptic ulcer disease. Eradication treatment was given with omeprazole, tetracycline-HCL, metronidazole and colloidal bismuth subcitrate taken with the midday and evening meals for 10 days [2]. C-Urea Breath test was repeated 4–6 weeks after the end of treatment and all patients resulted cured. Serum pancreatic amylase and lipase levels were re-evaluated after 3, 6 and 10–12 months in two different laboratories and resulted persistently normal (Table 1). A potential role of H. pylori infection in several extraintestinal pathologies has been suggested [3] and a link between gastric infection by H. pylori and autoimmune pancreatitis has been hypothesized [4]. Interestingly, in a recent study, Helicobacter DNA was detected in pancreas, including tumor tissue and surrounding pancreas of 75% of patients with pancreatic cancer, and 60% of patients with chronic pancreatitis, suggesting a possible role of H. pylori in the development of chronic pancreatitis and pancreatic

Background: Helicobacter pylori is now recognised to be the major cause of antral gastritis and a risk factor for further development of gastric cancer. This infection results in local inflammation and a modification of gastric mucosal epithelial cell characteristics. Systematic investigation for the expression of the secretory component by gastric epithelium in a personal historical series of biopsy specimens showed the expression of this activation marker in 38% of the cases, 19% also showing clear signs of H. pylori infection. Aims: To further appreciate the activation of epithelial cells in the chronic gastric inflammation associated with H. pylori infection and other types of gastritis without consideration of the grade of gastritis. Methods: Punch gastric biopsies from 36 patients (10 patients with confirmed H. pylori gastritis, 16 patients with non-H. pylori gastritis and 10 controls) were tested for the expression of ICAM-1/CD54, HLA-DP, -DQ, -DR, secretory component and bcl-2 by immunofluorescence. Results: Up-regulation of most markers was observed both in H. pylori and non-H. pylori gastritis, although secretory component, CD54 and DP expression was more closely associated with H. pylori gastritis. Conclusion: H. pylori infection appears to activate gastric epithelial cells more strongly than other types of gastritis. This suggests an active relationship between this bacterium and epithelial cells. Investigation of the up-regulationship between this bacterium and epithelial cells. Investigation of the up-regulation of secretory component, ICAM-1/CD54 or DP in gastric biopsies may serve as extensive markers in search of H. pylori gastric infections.

Anti-Helicobacter pylori antibodies were determined in 157 institutionalised Cantonese children, mean age 9.5 +/- 3.9 (SD) years, with profound neurodevelopmental disabilities. Eighty-seven (55.4%) were H. pylori seropositive compared with four of 50 (8%, P > 0.0002) of an age-matched control group, mean age 7.2 +/- 4.3 (SD) years. Eight of 15 seropositive children with a recent history of upper gastrointestinal bleeding underwent endoscopy and in all cases gastric infection with H.pylori was confirmed. Anthropometric data from institutionalised children revealed marked malnutrition but showed no significant difference between seropositive and seronegative children. Disabled children receiving long-term residential care in Hong Kong are confirmed to be at increased risk of H.pylori infection.