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At least 19 recordsLinked to original sources
PubMedDate not supplied

Histologic characteristics of Campylobacter pylori (Helicobacter pylori) mediated gastritis.

One hundred-nineteen specimens were reviewed to determine whether or not there were histologic changes specific for Campylobacter pylori (CP), (Helicobacter pylori) mediated gastritis. Hematoxylin and eosin (H&E), Brown-Hopp, and Wright-Giemsa stained sections were examined independently by two pathologists for (a) the presence of acute cryptitis, (b) percent and degree of crypt involvement, and (c) spectrum of inflammatory cells within the lamina propriae. The amount of mucus was quantified on the Periodic Acid Schift (PAS)-Alcian Blue stain sections. Changes in the character of the mucus were noted by using both the PAS-Alcian Blue and the High Iron Diamine-Alcian Blue. A positive specimen for Campylobacter pylori (CP+), (Helicobacter pylori) was defined as one in which curved or spiral shaped microbes were identified on Wright-Giemsa and Brown-Hopp stain. Seventy-eight specimens were CP+ and 41 CP-. Statistically significant histologic findings included the extent and degree of superficial cryptitis and the preponderance of plasma cells in CP+ cases. These findings confirm aspects seen in an animal model and suggest that there is an histologic pattern consistent with C. pylori (Helicobacter pylori) mediated gastritis.

Adult↗
PubMed2004

Intact gram-negative Helicobacter pylori, Helicobacter felis, and Helicobacter hepaticus bacteria activate innate immunity via toll-like receptor 2 but not toll-like receptor 4.

Molecular and genetic studies have demonstrated that members of the Toll-like receptor (TLR) family are critical innate immune receptors. TLRs are recognition receptors for a diverse group of microbial ligands including bacteria, fungi, and viruses. This study demonstrates that distinct TLRs are responsible for the recognition of Helicobacter lipopolysaccharide (LPS) versus intact Helicobacter bacteria. We show that the cytokine-inducing activity of Helicobacter LPS was mediated by TLR4; i.e., TLR4-deficient macrophages were unresponsive to Helicobacter pylori LPS. Surprisingly, the cytokine response to whole Helicobacter bacteria (H. pylori, H. hepaticus, and H. felis) was mediated not by TLR4 but rather by TLR2. Studies of HEK293 transfectants revealed that expression of human TLR2 was sufficient to confer responsiveness to intact Helicobacter bacteria, but TLR4 transfection was not sufficient. Our studies further suggest that cag pathogenicity island genes may modulate the TLR2 agonist activity of H. pylori as cagA+ bacteria were more active on a per-cell basis compared to cagA mutant bacteria for interleukin-8 (IL-8) cytokine secretion. Consistent with the transfection studies, analysis of knockout mice demonstrated that TLR2 was required for the cytokine response to intact Helicobacter bacteria. Macrophages from both wild-type and TLR4-deficient mice produced a robust cytokine secretion response (IL-6 and MCP-1) when stimulated with intact Helicobacter bacteria. In contrast, macrophages from TLR2-deficient mice were profoundly unresponsive to intact Helicobacter stimulation, failing to secrete cytokines even at high (100:1) bacterium-to-macrophage ratios. Our studies suggest that TLR2 may be the dominant innate immune receptor for recognition of gastrointestinal Helicobacter species.

Animals↗
PubMed1994

Healing of protein losing hypertrophic gastropathy by eradication of Helicobacter pylori--is Helicobacter pylori a pathogenic factor in Ménétrier's disease?

Hypertrophic gastropathy--that is, Ménétrier's disease--was found, in a retrospective analysis, to be associated with Helicobacter pylori in more than 90% of patients. It is proposed that hypertrophic gastropathy represents a special form of H pylori gastritis in these patients. A case is described of a 28 year old woman with Ménétrier's disease associated with proved protein loss from the stomach. Treatment with cimetidine for more than three years had little benefit when colonisation by H pylori was detected. Density of H pylori colonisation and activity of gastritis, which was also present in the first biopsy specimens taken five years ago, were more pronounced in the body than in the antrum, which is in agreement with the characteristics of H pylori gastritis found in other cases with Ménétrier's disease. A 14 day antibacterial treatment course with 750 mg amoxicillin three times a day combined with 40 mg omeprazole three times a day was started in April 1991. This resulted in eradication of H pylori and the return to normal of giant folds and the mucosal histology. Serum protein concentrations returned to normal within six weeks and remained normal at two endoscopies during a two year follow up. This case report suggests that a subgroup of the patients with Ménétrier's disease may be healed by the eradication of H pylori.

Adult↗
PubMed1999

Differential features of gastric cancer patients, either Helicobacter pylori positive or Helicobacter pylori negative.

BACKGROUND: Helicobacter pylori infection is associated with an increased risk of gastric cancer. In Helicobacter pylori negative patients, factors different from those in Helicobacter pylori positive patients may be involved in gastric carcinogenesis. METHODS: Thirty-nine recently diagnosed consecutive patients with gastric cancer were investigated. Gastric biopsies were obtained for detection of Helicobacter pylori (by immunohistochemistry), non-Helicobacter pylori flora (by modified Giemsa and culture) and histological assessment according to the Sydney classification by Haematoxylin-Eosin staining. In serum samples, Helicobacter pylori antibodies were determined by IgG enzyme-linked immunosorbent assay, IgA enzyme-linked immunosorbent assay, and Western blotting. Furthermore, serum gastrin, pepsinogen A and C and plasma chromogranin A were determined. RESULTS: Helicobacter pylori was detected by immunohistochemistry in 53.8%, by IgG in 56.4%, by IgA in 33.3%, and by Western blotting in 74.4% of the 39 patients. Ten patients (25.6%) were negative by both histology and serology. Non-Helicobacter pylori flora was detected in 27 of the 39 patients (69.2%) with a similar frequency in Helicobacter pylori positive and negative patients. Helicobacter pylori positivity was found significantly more often in diffuse than intestinal type carcinoma patients (p < 0.05). Elevated gastrin levels and antrum-sparing atrophic gastritis were more frequent in Helicobacter pylori negative than in Helicobacter pylori positive patients (p < 0.05). CONCLUSIONS: In 10 out of 39 gastric cancer patients, no evidence of previous or current Helicobacter pylori infection could be demonstrated. Non-Helicobacter pylori was found in 69.2% of patients regardless of the Helicobacter pylori status. Further studies are needed to establish the contribution of non-Helicobacter pylori flora as well as antrum-sparing atrophic gastritis with hypergastrinaemia to the development of gastric cancer.

Aged↗
PubMed1999

Growth characteristics and influence of antibiotics on rough/smooth phenotypic variants of Helicobacter pylori.

Helicobacter pylori shows a rather high variability of several biochemical markers including lipopolysaccharide structures. This study aimed to determine whether Helicobacter pylori has a potential for phenotypic variability and to describe its effects on bacterial pathogenesis. From colonies of three clinical strains of Helicobacter pylori with rough (R) colony morphology, spontaneous phenotypic variants with smooth (S) colony morphology were isolated that occurred with a frequency of 10(-2) to 10(-3), irrespective of growth conditions. R-variant bacteria produced exclusively low-molecular-mass lipopolysaccharide. They exhibited increased lysis in the presence of plain air. In contrast, the S variants produced low- and high-molecular-mass lipopolysaccharide and did not exhibit increased lysis in the presence of plain air. Cocultivation of bacterial cells with AGS stomach cancer cells revealed that R-variant bacteria but not S-variant bacteria effected an inhibition of high molecular-weight glycoprotein biosynthesis and secretion by the host cells. Skirrow supplement added as selective agent to liquid and/or solid media was tolerated to a similar extent among R- and S-variant bacteria, while all variants proved sensitive to metronidazole, amoxicillin and clarithromycin except for the R and S isolates of strain Hp57, which showed resistance to the latter compound. It was concluded that R- and S-variants of Helicobacter pylori may have distinct roles in pathogenesis; nevertheless, these bacteria may be isolated by traditional methods and eradicated by conventional anti-infective therapy.

Anti-Bacterial Agents↗
PubMed2002

[Hormonal regulation of gastric secretion and Helicobacter pylori].

Helicobacter pylori has been recognized as one of the most important factors that lead to chronic changes in the gastric mucosa. These changes have either direct or indirect impact on various intestinal hormones (gastrin, somatostatin, bombensin, cholecystokinin...) which regulate gastric secretion. Gastric secretion enhancement is mostly caused by higher concentration of serum gastrin. The mechanism in which the Helicobacter pylori infection influences the regulation of gastrin and other intestinal hormones is yet to be discovered. It is known that eradication of the Helicobacter pylori infection decreases serum gastrin concentration, thus decreasing gastric secretion and inflammatory changes of the gastric mucosa.

Gastric Acid↗
PubMed2005

A novel colorimetric broth microdilution method to determine the minimum inhibitory concentration (MIC) of antibiotics and essential oils against Helicobacter pylori.

Helicobacter pylori infections have been associated with the pathogenesis of a number of stomach and gastroduodenal diseases. In order to find alternative drugs for their treatment the search is increasingly focused on new antimicrobial products. However, no standardized methods are available to test the anti-Helicobacter pylori activity in particular of natural substances. Therefore we developed a broth microdilution assay to investigate the susceptibility of this fastidious slow growing bacterium against 15 essential oils widely used to treat disorders of the gastrointestinal tract. The MIC values were determined colorimetrically using p-iodonitrophenyltetrazolium violet (INT) as an indicator for bacterial cell viability. The test sytem was evaluated with three common antibiotics: amoxicillin, ampicillin and levofloxacin. The antibiotic MICs were controlled by Etest. The Helicobacter reference strain was remarkably susceptible to both the antibiotics (amoxicillin MIC: 0.02 microg/ml, ampicillin MIC: 0.064 microg/ml, levofloxacin MIC: 0.39 microg/ml) and the essential oils. Most of their MICs ranged from 0.015 to 0.064% (v/v) and about 140.0 to 280.0 microg/ml, respectively. Interestingly, chamomile oil, orange flower oil and ginger oil inhibited the bacterial growth in extraordinarily low concentrations of 0.0075% (v/v) and about 65 microg/ml, respectively. The bactericidal concentrations were generally one to two dilution steps higher. In conclusion, we could develop an innovative assay for the MIC determination of essential oils and antibiotics against Helicobacter pylori, which is simple to handle, accurate, reproducible and not as time- and material-consuming as traditional agar dilution techniques.

Anti-Bacterial Agents↗
PubMed1996

Triple therapy and Helicobacter pylori.

Helicobacter pylori is becoming increasingly important as a gastrointestinal pathogen and aetilogical agent in several disease states. This review attempts to clarify the role of Helicobacter pylori and importantly, simplify treatment options.

Amoxicillin↗
PubMed1994

Helicobacter pylori.

Helicobacter pylori is the cause of chronic active gastritis. It is integral to the pathogenesis of peptic ulcer disease and is epidemiologically linked to gastric cancer and lymphoma. Helicobacter pylori can be detected through a variety of invasive (urease testing, culture, or histologic diagnosis of endoscopic biopsies) and noninvasive (urease breath tests, serologic tests) diagnostic tests. It is now appropriate to detect and eradicate H pylori in patients with a peptic ulcer as the natural history of peptic ulcer disease is then markedly improved. At this time, there is no role for H pylori eradication in the prevention of gastric cancer; however, this concept is being actively investigated. There is no indication to treat patients who have H pylori and nonulcer dyspepsia or gastritis because eradication does not reliably affect their symptoms. Current regimens for eradication include bismuth, antibiotics, and antisecretory agents. Complex and poorly tolerated regimens (triple therapy) may no longer be necessary, as simpler regimens (omeprazole and amoxicillin or clarithromycin) appear to be as effective and better tolerated.

Gastritis↗
PubMed1991

Flocculation of venereal disease research laboratory reagent by Helicobacter pylori.

Helicobacter pylori strains flocculated with Venereal Disease Research Laboratory (VDRL) reagent in a glass slide test. Other pathogenic bacterial and fungal strains were nonreactive. The specific VDRL reaction property of Helicobacter pylori indicates an affinity of the cells for lipoidal substances, and can be used as a diagnostic aid for species identification.

Bacteria↗
PubMedDate not supplied

Evaluation of salivary antibodies to detect infection with Helicobacter pylori.

Helicobacter pylori infection is an important cause of peptic ulcer disease and chronic gastritis. Infection with this bacterium stimulates the production of immunoglobulin (Ig) G antibody. Salivary IgG antibody tests to detect H pylori infection offer a convenient and noninvasive method of diagnosis. To evaluate an IgG salivary antibody kit, saliva was collected from 157 out-patients with dyspepsia referred for endoscopy to a tertiary centre. A salivary IgG ELISA antibody assay was performed using the Helisal Helicobacter pylori (IgG) assay kit, and at least four gastric biopsies were obtained. H pylori infection was confirmed by demonstration of the organism on Warthin-Starry silver stain (sensitivity 85%, specificity 55%). The prevalence of infection with H pylori was 30%. When the analysis was redone, excluding those treated with eradication therapy, the results were similar (sensitivity 86%, specificity 58%). The positive predictive value of the assay was 45% and the negative predictive value was 90%. Despite the ease of sampling, the assay used has limited diagnostic utility, lacking the predictive value to indicate which patients referred with dyspeptic symptoms to a tertiary care setting are infected with H pylori.

Adolescent↗
PubMed1998

[Remission ratio of chronic urticaria--"spontaneous" healing or result of eradication of Helicobacter pylori?].

Helicobacter pylori infection has been assumed to be the underlying cause of some dermatological diseases such as, chronic urticaria. In order to investigate this problem we interviewed 55 patients with chronic urticaria concerning the state of the disease approximately 10 months after being discharged from hospital. After an additional six months we interviewed them for a second time and thus determined the remission ratio. There was no significant evidence showing that a link exists between urticaria and proven Helicobacter pylori infection (chi 2-Test). There was also no significant correlation in the remission ratio between patients treated with a triple therapy and non-treated patients (exact Fisher-Test).

Chronic Disease↗
PubMed1993

Cell-associated haemolytic activity of Helicobacter pylori.

Helicobacter pylori cells cultured on solid medium were quantitatively tested for haemolytic activity against erythrocytes of man, sheep, the guinea pig and rabbit. Using 4-day and 8-day cultures of two standard strains (ATCC 43504, IMMi 676), human erythrocytes were not lysed by 10% bacterial suspensions. Rabbit erythrocytes were the most sensitive to 8-day cultures. Hot-cold incubation yielded the highest haemolysis titres. The extent of haemolysis strongly correlated with the number of bacterial cells. Supplementation of the test medium (PBS, pH 7.4) with L-cysteine, dithiothreitol, MgCl2, EDTA, cholesterol, lecithin or sphingomyelin did not influence the haemolysis titres. They were significantly reduced in the presence of pronase E, human serum, bovine serum albumin or CaCl2, and by heat treatment of the bacteria. Supplementation of the test medium with cardiolipin strongly increased the haemolysis titres. Comparing the cell-associated haemolytic activity of 18 strains, the titres ranged from < 2 to 64, with a median titre of 16. No correlation was found between the haemolytic activity and phospholipase C activity of the cell suspensions. It was concluded that the formation of lysophosphatides and non-enzymatic factors rather than a sulphydryl-activated cytolysin or phospholipase C are responsible for the cell-associated haemolytic activity. This property may be involved in the pathogenicity and virulence of Helicobacter pylori.

Animals↗
PubMed1997

What is the role for vaccination in Helicobacter pylori?

Helicobacter pylori has been implicated in the etiology of peptic ulcer disease, chronic gastritis, gastric carcinoma, and gastric mucosa-associated lymphoid tissue lymphoma. Although significant progress has been made in treating this infection with combinations of either antimicrobial agents or antimicrobial agents plus proton pump inhibitors, these antimicrobial-based treatments continue to be suboptimal. Over the past few years it has become increasingly recognized that direct mucosal immunization can induce protection from infection at mucosal surfaces. Therefore, prevention of H. pylori infection by oral immunization is an alternative approach for the control of H. pylori disease. Using the Helicobacter felis mouse model or H. pylori mouse model, both prophylactic and therapeutic oral immunizations have been shown to be effective against H. pylori. In addition, several H. pylori proteins have been identified as potential candidate vaccines, and a phase 1 clinical trial has been completed that demonstrates the safety and tolerability of urease as a vaccine antigen. Such antigens in combination with a safe mucosal adjuvant could be used in the form of an oral vaccine administered during childhood before exposure to H. pylori to prevent infection. In addition, therapeutic immunization alone or as an adjunct to antimicrobial therapy may be capable of achieving a cure rate approaching 100%.

Animals↗
PubMedDate not supplied

Clinical onset of the Crohn's disease after eradication therapy of Helicobacter pylori infection. Does Helicobacter pylori infection interact with natural history of inflammatory bowel diseases?

BACKGROUND: There are conflicting reports concerning the prevalence of Helicobacter pylori infection in patients with inflammatory bowel diseases: some studies connected Sulphasalazine therapy and lower incidence of Helicobacter pylori infection, but others showed lower prevalence of Helicobacter pylori infection in inflammatory bowel diseases despite the choice of therapy. CASE REPORT: A 28-year-old male patient presented in January 1996 with the symptoms of ulcer like dyspepsia. There was no significant abnormality on physical examination, laboratory testing and abdominal ultrasound. Histology examination of the biopsy specimen taken during the upper endoscopy revealed Helicobacter pylori associated active gastritis only in the corporal part of the stomach. After two weeks eradication therapy (Omeprazole, Amoxicillin) he was well. Three months later, at the control endoscopy, granulomatous gastritis of the corporal localization was detected, without Helicobacter pylori present. Antral mucosa appeared normal, both, on endoscopy and histology examination. In July 1996 he started with cramping abdominal pain, mild periodical fever and episodes of watery diarrhea. In laboratory results we found nonspecific signs of inflammation. We repeated upper endoscopy, colonoscopy and enteroclysis--with evidence of segmental stenotic lesions of the upper part of ileum and jejunum. Again, we confirmed granulomatous gastritis and small granuloma in the proximal jejunum. After starting the 5-ASA therapy in combination with Metronidazol, patient was better clinical condition, and laboratory results were normal. We suggested mesalamine maintenance therapy 1 gr. every day, and three years later he is well, in clinical remission of Crohn's disease. CONCLUSION: The clinical course of the Crohn's disease maybe "sui generis" connected with Helicobacter pylori infection- but the exact mechanisms remain to be discovered.

Abdominal Pain↗
PubMedDate not supplied

Production of a cytotoxin by Helicobacter pylori.

Helicobacter pylori produces a cytotoxin that was initially detected as the ability of broth culture filtrates of this bacterium to induce intracellular vacuolation of cultured cells. Fifty-three percent of more than 200 isolates of H. pylori tested produce the cytotoxin, which appears to be unique to H. pylori. Results of characterization studies suggest that the cytotoxin is a high-molecular-weight protein. Detection of serum antibody to the cytotoxin by neutralization or immunoblotting indicates that this toxin is produced in vivo. The cytotoxin is more frequently associated with cases of peptic ulceration than with cases of gastritis; this finding suggests that the toxin contributes to the severity of disease associated with H. pylori infection.

Cytotoxins↗
PubMed1996

Transmission and epidemiology of Helicobacter pylori.

Helicobacter pylori is one of the most common bacterial infections worldwide. However, the majority of those infected do not develop clinical manifestations of disease. This review discusses the epidemiology of the organism in terms of incidence and prevalence, the presumed means of transmission from person to person, and how typing of the organism has helped the epidemiologist. The epidemiology of disorders that are associated with H. pylori is also discussed.

Helicobacter Infections↗