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PubMed2003

Role for complement in development of Helicobacter-induced gastritis in interleukin-10-deficient mice.

The mechanisms by which the immune response can eradicate gastric Helicobacter infection are unknown. We hypothesized that Helicobacter-induced activation of the complement system could promote both inflammation and eradication of Helicobacter from the stomach. In vitro studies demonstrated that Helicobacter felis activates complement in normal mouse serum but not in serum from Rag2(-/-) mice, indicating that H. felis activates complement through the classical pathway. Next, we infected complement-depleted wild-type control and interleukin-10-deficient (IL-10(-/-)) mice with H. felis. Helicobacter infection of wild-type mice elicited a mild, focal gastritis and did not alter serum complement levels. Infection of IL-10(-/-) mice with H. felis elicited severe gastritis. After the initial colonization, the IL-10(-/-) mice completely cleared Helicobacter from the stomach by day 8. In contrast to wild-type mice, H. felis-infected IL-10(-/-) mice had a marked increase in serum complement levels. Complement depletion of wild-type mice did not affect the intensity of gastric inflammation or the extent of Helicobacter colonization compared to that for the wild-type control mice. In contrast, complement depletion of Helicobacter-infected IL-10(-/-) mice decreased the severity of gastritis, decreased the Helicobacter-induced infiltration of neutrophils into the stomach, and delayed the clearance of bacteria. In vitro studies of stimulated splenocytes and neutrophils from IL-10(-/-) mice produced a twofold increase in complement production compared to that for wild-type mice. Pretreatment with IL-10 inhibited this increase. These studies identify a role for complement in the local immune response to gastric Helicobacter in IL-10(-/-) mice and suggest a role for IL-10 in the regulation of complement production.

Animals↗
PubMedDate not supplied

Helicobacter infection in dogs and cats: facts and fiction.

The discovery of the spiral bacterium Helicobacter pylori and its causative role in gastric disease in humans has brought a dramatic change to gastroenterology. Although spiral bacteria have been known for more than a century to infect the stomachs of dogs and cats, recent research has been conducted mainly in the wake of interest in H. pylori. H. pylori has not been found in dogs and only very rarely in cats and zoonotic risk is minimal. A variety of other Helicobacter spp. can infect the stomach of pets; however, their pathogenic role is far from clear, and they have a small but real zoonotic potential. The prevalence of gastric Helicobacter spp. in dogs and cats is high, irrespective of clinical signs, and as in human medicine, mode of transmission is unclear. The relationship of Helicobacter spp. to gastric inflammation in cats and dogs is unresolved, with inflammation, glandular degeneration, and lymphoid follicle hyperplasia accompanying infection in some but not all subjects. Circulating anti-Helicobacter immunoglobulin G antibodies have been detected in 80% of dogs with naturally acquired infection and most dogs and cats with experimental infection. The gastric secretory axis is similar in infected and uninfected cats and dogs and no relationship of infection to gastrointestinal ulcers has been found. Differences in the pathogenicity of Helicobacter spp. are apparent, because infection with H pylori is associated with a more severe gastritis than infection with other Helicobacter spp. in both cats and dogs. Rapid urease test, histopathology, and touch cytology are all highly accurate invasive diagnostic tests for gastric Helicobacter-like organisms in dogs and cats, whereas culture and polymerase chain reaction are the only means to identify them to the species level. Urea breath and blood tests or serology can be used to diagnose Helicobacter spp. noninvasively in dogs and cats. Most therapeutic studies in pets have not shown long-term eradication of Helicobacter spp. Whether this is due to reinfection or recrudescence has not been established.

Animals↗
PubMed1991

Gastric Helicobacter and upper gastrointestinal symptoms in chronic renal failure.

We studied histologically antral biopsies from 89 consecutive patients with chronic renal failure for Helicobacter pylori (previously Campylobacter pylori). A dose-response gastric secretion test was also performed. The frequency of Helicobacter-positive subjects was low (15/89, 17%), corresponding to figures reported in the literature for young symptomless volunteers. Helicobacter-positive patients had significantly more frequently upper gastrointestinal symptoms than Helicobacter-negative individuals (P less than 0.05). Antral gastritis was more common in the Helicobacter-positive than in the Helicobacter-negative renal patients (P less than 0.01), but the incidence of body gastritis did not differ between them. The Helicobacter-positive patients had lower serum urea levels (P less than 0.01) and higher acid outputs (P less than 0.001) than Helicobacter-negative subjects. All patients had raised fasting serum gastrin levels, which possibly obscured the difference between Helicobacter-positive (283 pg/ml) and -negative (331 pg/ml) patients. We conclude that in chronic renal failure gastric colonization of Helicobacter pylori is not more frequent than usual. It correlates positively with antral gastritis, gastric acid output and upper gastrointestinal symptoms, but negatively with serum urea levels.

Biopsy↗
PubMedDate not supplied

[Helicobacter pylori infection and a decrease in the pH of gastric juice as a possible cause of bleeding in erosive gastritis].

INTRODUCTION: Bleeding erosive gastritis and ulcer disease are the most common causes of bleeding from the upper parts of the alimentary tract. Over the period of the last 10 years there has been an increased number of patients where Helicobacter pylori is mentioned as the possible cause of infection. At the same time in this group of patients pH values were decreased. During our research we wanted to examine the influence of local pH value and Helicobacter pylori infection on the occurrence of bleeding erosive gastritis. MATERIAL AND METHODS: During this research we examined two groups of patients. The following parameters were examined within these two groups of patients: 1. presence of Helicobacter pylori infection; 2. histopathologic changes in mucus; 3. there were 57 patients with a bleeding form of gastritis of unknown etiology, whereas the second group consisted of 351 patients with non-bleeding form of gastritis. We examined the localization: 4. local pH. RESULTS: The presence of Helicobacter pylori infection is statistically significantly higher in the group of patients with bleeding gastritis, when compared to the non-bleeding group (72%:57%). Within the Helicobacter positive patients the most common change of mucose (over 90%) is active chronic gastritis. The presence of erosions and histopathological changes characteristic for Helicobacter pylori infection coincides with colonization of Helicobacter in the antrum. The pathogenetic action of bacteria in antrum decreases the local pH. Therefore the lowest value of local pH occurred in the group of bleeding Helicobacter pylori positive gastritis (1.72). DISCUSSION: Results of this research helped us in treatment of helicobacter pylori positive patients making a risk group for development of recurrent bleeding. We accomplished therapeutical effect in 80% of patients by using a three component eradication therapeutic protocol for helicobacter pylori. Within the group of patients who have been cured, regression of histopathological changes occurred and increase of local pH took place. In the group with persistent infection we have come across with high percentage of recurrent bleeding (37.5%). CONCLUSION: In our opinion helicobaceter pylori infection and decrease of local pH, which take place during the reaction of mucose on the presence of infection, are very aggressive factors which can cause bleeding erosions.

Adult↗
PubMedDate not supplied

Prevalence of Helicobacter pylori in the residual stomach after gastrectomy for gastric cancer.

BACKGROUND/AIMS: In recent years, the role of Helicobacter pylori in gastritis of the residual stomach has attracted much attention. We investigated the prevalence of Helicobacter pylori in the residual stomach after distal gastrectomy for gastric cancer, as well as the correlations between Helicobacter pylori positivity and clinical characteristics or the severity of gastritis in the residual stomach. METHODOLOGY: The subjects were 66 patients with gastric cancer who underwent distal gastrectomy with Billroth I reconstruction at our department. Helicobacter pylori was detected by the 13C-urea breath test, and patients were considered to be Helicobacter pylori-positive if the delta 13C value was > 2.5@1000. RESULTS: The overall Helicobacter pylori positivity rate of the gastrectomy patients was a high 80.3%, with the rate being especially high in patients under 60 years of age and in those tested less than 5 years after surgery. There was a close relationship between Helicobacter pylori positivity and the severity of gastritis. CONCLUSIONS: Helicobacter pylori infection appears to cause the development of gastritis. Helicobacter pylori eradication needs to be taken into consideration in the management of Helicobacter pylori-positive patients after gastrectomy.

Age Factors↗
PubMedDate not supplied

Histological and clinical predictive value of determination of tissue CagA status by PCR in Helicobacter pylori infected patients; results of the large population based study in western Turkey.

BACKGROUND/AIMS: Early experimental and epidemiological studies have suggested that the presence of cagA gene was a virulence factor for Helicobacter pylori. We aimed to investigate the clinical significance of tissue CagA status in Helicobacter pylori infected patients and to assess its association with histological changes in gastric mucosa. METHODOLOGY: Three hundred and forty-five patients with Helicobacter pylori infection established by both urease test and histological examination were included in the study. The symptoms of the patients were recorded according to the Glasgow dyspepsia scale. Biopsies (cardia, corpus, angulus and antrum) were evaluated histologically according to the Sidney system. The cagA status was determined by polymerase chain reaction method from an antral biopsy. Polymerase chain reaction studies were performed by Wizard genomic DNA purification system (promega). We also determined the serum levels of tumor necrosis factor-alpha, and gastrin. They were all prescribed lansoprazole (30 mg b.i.d.), clarithromycin (500 mg b.i.d.), and amoxycillin (1 g b.i.d.) for a week. At the 8th week a second endoscopy was performed and further biopsy specimens were obtained from the same sites. Mann-Whitney U and chi 2 tests were used for statistical analyses. RESULTS: Two hundred and thirty-five patients (68.1%) were infected with cagA-positive strains of Helicobacter pylori and the other 110 patients (31.8%) were infected with cagA-negative strains. We compared the parameters and measurements studied in this trial between the patients infected with cagA-positive and negative Helicobacter pylori strains. Helicobacter pylori density was greater in the cagA-positive group by 1.9 +/- 0.9 than in the cagA-negative group by 1.2 +/- 0.7 (P = 0.01). Helicobacter pylori activity and chronic inflammation also were significantly higher in the cagA-positive group with the values of 1.4 +/- 0.8 and 2.1 +/- 1.1 than in the cagA-negative group with 0.7 +/- 0.2 and 1.3 +/- 0.5, respectively (P = 0.001, P = 0.002). The presence of atrophy and lymphoid aggregate was not different between the two groups (P > 0.05). However intestinal metaplasia was shown to be significantly frequent in patients infected with cagA-positive Helicobacter pylori strains (0.001). Serum tumor necrosis factor-alpha and gastrin levels which were accepted as the markers of inflammation in Helicobacter pylori infection were increased in the cagA-positive group compared with the cagA-negative group. Serum tumor necrosis factor-alpha level was 11.3 +/- 7.0 pg/mL in the cagA-positive group and 4.9 +/- 2.7 pg/mL in the cagA-negative group (P = 0.001). Gastrin level also showed a significant difference between two groups by 66.8 +/- 31.1 pg/mL and 37.2 +/- 19.2 pg/mL, respectively, in the cagA-positive and negative groups (P = 0.001). The virulent strains seem to cause peptic ulcer more frequently. Peptic ulcer was determined in 17% of patients in the cagA-positive group but this ratio was 9% in the cagA-negative group (P = 0.608). Although, all these differences of the degree of inflammation, clinical spectrum and biochemical parameters were seen, interestingly there was no significant difference in the severity of the symptoms of the patients in both groups according to Glasgow dyspepsia severity score (P = 0.20). CONCLUSIONS: Our results confirm that cagA-positive strains of Helicobacter pylori cause greater histological changes. However this virulence is not associated with more severe symptoms. The histological changes can be predictable by determining the tissue cagA status.

Adult↗
PubMed2005

[Association between Helicobacter infection in liver tissue and primary liver carcinoma].

OBJECTIVE: To investigate the relationship between Helicobacter species and primary liver carcinoma (PLC). METHODS: The liver samples resected during operation from 21 patients with PLC diagnosed by histopathology and 12 patients with other liver diseases as controls were studied. Helicobacter species in liver specimens from the studied subjects were examined by PCR with Helicobacter specific 16SrRNA primers. The amplified products were identified by Southern hybridization and nucleic acid hybridization in situ and sequencing. The specimens were made slices to undergo in situ hybridization of cDNA-mRNA of Helicobacter. Qualitative and quantitative studies were used to assess the correlation of liver tissue helicobacter infection with PLC. RESULTS: Thirteen of the 21 samples (62%) of PLC were positive for Helicobacter specific 16SrRNA gene, while none was positive in the controls (P < 0.01). In situ hybridization results demonstrated a highly Helicobacter 16SrRNA-mRNA positive rate in the PLC group (62%) and none of positive specimen in the control group (P < 0.01). Nine of the Helicobacter specific PCR applicants were sequenced and a homology of 97.80% in comparison with 16SrRNA of H p was found. CONCLUSION: Helicobacter infection may exist in the liver tissues of PLC patients with a high infection rate, suggesting an association between Helicobacter infection and PLC.

Adult↗
PubMed2006

[Helicobacter pylori does not contribute to iron deficiency in hemodialysis patients].

BACKGROUND: Many studies in the general population have shown a link between Helicobacter pylori infection and iron-deficiency, often resulting in iron-deficient anaemia. Despite the high prevalence of iron deficiency in hemodialysis patients, no studies have been performed in this population. OBJECTIVE: To evaluate the role of Helicobacter pylori infection in the appearance of anemia and the iron requirements in our hemodialysis population. MATERIAL AND METHODS: After excluding patients with severe pathology and short life expectancy and those with blood losses secondary to other causes, 79 patients were included.Iron requirements and anaemia were determined by iron serum, ferritin, and hematocrit values; and by transfusion, eritropoietin and iron requirements. The diagnosis of Helicobacter pylori status was established by the concordance of at least two of the three non invasive diagnostic methods performed (breath test, serology and fecal antigen of Helicobacter pylori). RESULTS: Prevalence of Helicobacter pylori infection was 43%. No significant differences between patients infected or not by Helicobacter pylori were found in any of the variables analysed: hematocrit (33.5% versus 34.1%), serum iron (58.9 versus 63.7 pg/dl), ferritin(340.3 versus 264.2 ng/ml), transferrin saturation index (22.5% versus 25.2%), dose of eritropoietin administered (96.6 versus 93.5 U/kg/weekly), and parenteral iron (1,389 versus 1,538 mg/year). A noteworthy finding was that patients with Helicobacter pylori infection had been on hemodialysis for a shorter period than those without (37.4 versus 63.7 months,p = 0.04). CONCLUSION: Helicobacter pylori infection has no effect on anaemia (hematocrit, Eritropoietin dose or iron needs) in our hemodialysis patients. Prevalence of Helicobacter pylori is lower in patients with longer time on dialysis. We consider that the diagnosis of Helicobacter pylori infection must be reserved for clinical peptic ulcer suspicion or patients on transplant waiting list.

Aged↗
PubMed1998

Helicobacter pylori and plasma ammonia levels in cirrhotics: role of urease inhibition by acetohydroxamic acid.

BACKGROUND AND AIMS: The role of Helicobacter pylori as a cause of hyperammonaemia in cirrhotics has still not been fully clarified. This study was aimed at evaluating the effect of acute Helicobacter pylori urease inhibition by oral acetohydroxamic acid administration on blood ammonia levels in cirrhotic patients. METHODS: Twenty-nine cirrhotics (14 males, 15 females; mean age: 63 years; Child-Pugh class: 14 A, 9 B, and 6 C) undergoing upper gastrointestinal endoscopy were enrolled in the study. The presence of Helicobacter pylori infection was assessed by rapid urease test and histology. A semi-quantitative grading of bacterial density was also performed at histology. All patients received oral acetohydroxamic acid 750 mg, and blood samples for assessment of ammonia levels were taken before and at 15, 30, 60 and 90 minutes after administration. RESULTS: Helicobacter pylori infection was detected in 20 patients, while 9 patients were uninfected. Acetohydroxamic acid administration led to a significant reduction in blood ammonia levels at 15 and 30 minutes (mean +/- SD, 113 +/- 44 vs 101 +/- 43 and 93 +/- 38 micrograms/dl, respectively; p = 0.002) only in patients with Helicobacter pylori infection. Moreover, the reduction was statistically significant only in Child-Pugh B/C class patients and in those with moderate/marked Helicobacter pylori density in gastric mucosa. Basal ammonia levels did not differ between Helicobacter pylori positive and negative patients, nor in patients with mild and moderate/marked Helicobacter pylori density in gastric mucosa, while Child-Pugh class B/C cirrhotics had higher basal ammonia levels than class A cirrhotics, in both Helicobacter pylori positive and negative groups. CONCLUSIONS: Our data showed that Helicobacter pylori urease inhibition by acetohydroxamic acid administration significantly reduces blood ammonia levels in patients with more advanced liver cirrhosis and in those with a high bacterial density in gastric mucosa.

Aged↗
PubMed1998

Prevalence of gastric metaplasia in the duodenal bulb and distribution of Helicobacter pylori in the gastric mucosa. A clinical and histopathological study in 96 consecutive patients.

BACKGROUND: Consecutive untreated patients with duodenal ulcer (n = 49) or gastric ulcer (n = 47) were compared with regard to the presence of gastric metaplasia in the duodenal bulb, gastric distribution of Helicobacter pylori and histopathological findings to assess differences which may contribute to either duodenal ulcer or gastric ulcer development. METHODS: Serial sections of corpus, antral and duodenal mucosal biopsies were stained by haematoxylin-eosin stain for histopathological evaluation, immunohistochemistry for the detection of Helicobacter pylori, and duodenal biopsies alone by the PAS/Alcian blue stain to assess the presence of gastric metaplasia in the duodenal bulb. RESULTS: Helicobacter pylori was found in 81.6% of duodenal ulcer and in 83.0% of gastric ulcer patients. In duodenal ulcer and gastric ulcer patients, Helicobacter pylori was found in 79.6% and 79.5% of corpus, 77.6% and 72.3% of antral, and 16.7% and 20.0% of duodenal bulb biopsies, respectively. In duodenal ulcer patients, the density of Helicobacter pylori was significantly lower in corpus compared to antrum biopsies (p < 0.001). Furthermore, the Helicobacter pylori density was higher in corpus of gastric ulcer than of duodenal ulcer patients. Inflammatory scores followed the density of Helicobacter pylori infection. In the duodenal bulb of both duodenal ulcer and gastric ulcer patients, the occurrence and extent of gastric metaplasia were comparable. Gastric metaplasia was present in 5 out of 8 Helicobacter pylori positive duodenal biopsies of duodenal ulcer patients and in 3 out of 9 Helicobacter pylori positive duodenal biopsies of gastric ulcer patients. CONCLUSIONS: No evidence was found for a role of gastric metaplasia in the differential pathogenesis of duodenal ulcer or gastric ulcer. Differences in the gastric topography of Helicobacter pylori density and inflammatory scores between duodenal ulcer and gastric ulcer may contribute to differences in development and presentation of both peptic ulcer conditions.

Adult↗
PubMed1998

Polyamine profile in human gastric mucosa infected by Helicobacter pylori.

BACKGROUND: Several studies have demonstrated increased gastric epithelial cell proliferation associated with Helicobacter pylori infection, which is reversed after bacterium eradication. Among the substances involved in cell proliferation and differentiation, polyamines are a group of polycations found in high concentrations both in normal and neoplastic cells. AIMS: Of the study were: a) to examine the influence of Helicobacter pylori infection on the polyamine profile in the gastric antrum and body, by comparing infected, to uninfected, patients, b) to evaluate the effect of successful and unsuccessful bacterium eradication on polyamine levels. PATIENTS AND METHODS: Twenty-six consecutive dyspeptic patients (20 Helicobacter pylori positive and 6 Helicobacter pylori negative) undergoing gastroscopy were enrolled. Polyamines were evaluated in antral and body biopsies by High Performance Liquid Chromatography. RESULTS: Antral and body biopsies from Helicobacter pylori positive patients contained higher polyamine levels than those from Helicobacter pylori negative subjects. In Helicobacter pylori positive patients, the baseline polyamine levels were higher in the antrum than in the body. In Helicobacter pylori negative subjects, levels in the two stomach regions were similar. After therapy, polyamine levels decreased in patients with successful eradication, whereas these levels remained unchanged in patients in whom infection persisted. CONCLUSIONS: These findings indicate enhanced antral cellular proliferation linked to the presence of Helicobacter pylori and add weight to the postulation of an association between Helicobacter pylori infection and increased risk of neoplastic changes in gastric antral mucosa. Differences in antral and body levels of polyamines may also be considered as a further indication of the different mucosal reactivity between the two regions of the stomach towards bacterial invasion.

Adolescent↗
PubMed2003

Increased prevalence of seropositivity for non-gastric Helicobacter species in patients with autoimmune liver disease.

Various Helicobacter species have been isolated from the stomach, intestinal tract and liver of a variety of mammalian and some avian species, and Helicobacter DNA has been detected in human bile and liver samples. An immunoblot assay was established to analyse serum antibody responses to non-gastric Helicobacter species in patients with autoimmune liver diseases, in comparison with healthy individuals. Sera from 36 patients with primary sclerosing cholangitis (PSC), 21 with primary biliary cirrhosis, 19 with autoimmune chronic hepatitis and 80 blood donors were analysed by immunoblot, using cell-surface proteins from Helicobacter pullorum, Helicobacter bilis and Helicobacter hepaticus as antigens. Prior to testing, sera were cross-absorbed with a whole-cell lysate of Helicobacter pylori. Antibody reactivity to various proteins of these three Helicobacter species was measured by densitometric scanning and results were processed by computer software to estimate antigenic specificity. Results were also compared with antibody response to H. pylori. For H. pullorum, reactivity to at least two of the proteins with molecular masses of 48, 45, 37, 20 and 16 kDa, for H. hepaticus, reactivity to the 76, 30 and 21 kDa proteins and for H. bilis, reactivity to the 22 and 20 kDa proteins, seemed to have high specificity. Positive immunoblot results with sera from patients with PSC to antigens of H. pullorum, H. bilis and H. hepaticus were found in 38, 22 and 25 % of cases, respectively, and from patients with other autoimmune liver diseases, in 30, 22 and 22 % of cases, respectively. Prevalence of serum antibodies to non-gastric Helicobacter species was significantly higher in patients with autoimmune chronic liver diseases than in healthy blood donors (P < 0.001). Increased antibody levels to enterohepatic Helicobacter species raise questions concerning an infectious role of these emerging bacterial pathogens in human autoimmune liver diseases.

Adult↗
PubMed2005

Natural colonization with Helicobacter species and the development of inflammatory bowel disease in interleukin-10-deficient mice.

BACKGROUND: The interleukin-10-deficient (IL-10-/-) mice maintained in specific-pathogen-free (SPF) conditions develop typhlocolitis when experimentally infected with Helicobacter species. However, there is limited information regarding the role of Helicobacter species that naturally colonize IL-10-/- mice in typhlocolitis development. The aim of this study was to examine in SPF IL-10-/- mice the association between natural colonization specific Helicobacter species and typhlocolitis development. MATERIAL AND METHODS: Cecum and proximal colon from 72 C57BL/6 x 129/Ola IL-10-/- mice (8-20 weeks old) were removed for DNA extraction and histologic evaluation. Genus-specific polymerase chain reaction- denaturing gradient gel electrophoresis (PCR-DGGE) and species-specific PCR were used to detect Helicobacter species. Mice were grouped by age, sex, and Helicobacter colonization status, and their histologic scores were compared. The development of clinical typhlocolitis was observed in a further 12 mice. RESULTS: Species-specific PCR showed that mice were colonized with Helicobacter ganmani and/or Helicobacter hepaticus. The PCR-DGGE detected H. ganmani, H. hepaticus and an H. ganmani-like organism. The histologic scores in mice colonized with H. hepaticus were significantly higher than that in mice colonized with H. ganmani. Male mice showed significantly higher histologic scores than female mice. Four of the 12 mice developed clinical typhlocolitis in 38 weeks. CONCLUSION: Natural colonization with different Helicobacter species was found in IL-10-/- mice within the same breeding colony. The severity of typhlocolitis differed according to the colonizing Helicobacter species. Furthermore, the rate of typhlocolitis development in IL-10-/- mice naturally colonized with Helicobacter species was significantly slower than that reported in experimentally infected mice.

Animals↗
PubMed1996

Lipid profile of Helicobacter spp.: presence of cholesteryl glucoside as a characteristic feature.

The lipid and fatty acid profiles of eight Helicobacter spp. (H. nemestrinae, H. acinonyx, H. canis, Helicobacter sp. strain CLO-3, "H. rappini" [Flexispira rappini], H. pametensis, Helicobacter sp. strain Bird-B, and Helicobacter sp. strain Bird-C) and the fatty acid profiles of five additional species (H. pylori, H. felis, H. muridarum, H. mustelae, and H. fennelliae) were analyzed and compared. A heterologous fatty acid profile was observed among the Helicobacter spp., and on that basis the species could be divided into two groups. Group A had 19-carbon cyclopropane fatty acid (19:0cyc) and tetradecanoic acid (14:0) as the major fatty acids, and group B characteristically lacked the 19:0cyc and had hexadecanoic acid (16:0) and octadecenoic (18:1) acids as the major fatty acids. The species of group A are primarily gastric colonizers, and those of group B are primarily intestinal colonizers. Seven of the eight species studied showed the unusual and characteristic presence of cholesteryl glucosides (CGs), and most of these seven showed a very large amount (9.7 to 27.4% of the weight of total extractable lipid). The types of CGs and their distribution in different species were as follows: cholesteryl-6-O-acyl-alpha-D-glucopyranoside (cholesteryl-6-O-tetradecanoyl-alpha-D-glucopyranoside in H. nemestrinae and mainly cholesteryl-6-O-dodecanoyl-alpha-D-glucopyranoside in "H. rappini"), cholesteryl-alpha-D-glucopyranoside (H. nemestrinae, H. acinonyx, H. canis, Helicobacter sp. strain CLO-3, and "H. rappini"), and cholesteryl-6-O-phosphatidyl-alpha-D-glucopyranoside (H. nemestrinae, H. acinonyx, H. canis, and Helicobacter sp. strain CLO-3). Besides this, we could also detect cholesteryl acyl glucoside in H. acinonyx, cholesteryl glucoside in Helicobacter sp. strains Bird-B and -C, and cholesteryl phosphatidyl glucoside in "H. rappini" and Helicobacter sp. strain Bird-C. A selective accumulation of free cholesterol was observed in the neutral lipid fractions. On the basis of the detection of CGs in 11 of the 13 species studied so far, the presence of CGs appears to be a characteristic feature of the genus Helicobacter. In view of this and also because of a simple and rapid detection method described herein, the CGs can be used as a valuable chemotaxonomic marker.

Cholesterol↗
PubMed2002

Helicobacter marmotae sp. nov. isolated from livers of woodchucks and intestines of cats.

Woodchucks (Marmota monax) have a high incidence of hepatocellular carcinoma (HCC) associated with chronic infection with woodchuck hepatitis virus (WHV) and serve as a model of hepatitis B virus-associated HCC in humans. Helicobacter hepaticus, an enterohepatic helicobacter in mice, is known to cause hepatocellular adenomas and carcinomas in susceptible mouse strains. In long-term chemical bioassays conducted with B6C3F(1) mice, H. hepaticus has been regarded as a confounding factor because of its tumor-promoting activity. In order to determine if woodchucks harbor a Helicobacter sp. that might play a role in potentiating hepatic inflammation or neoplasia, a study was undertaken to determine whether woodchucks' livers were infected with a Helicobacter sp. Frozen liver samples from 20 (17 WHV-infected and 3 noninfected) woodchucks, 10 with WHV-associated hepatic tumors and 10 without tumors, were cultured by microaerobic techniques and analyzed by using genus- and species-specific helicobacter PCR primers. A 1,200-bp Helicobacter sp.-specific sequence was amplified from 14 liver samples. Southern hybridization confirmed the specific identity of the PCR products. Nine of the 10 livers with tumors had positive Helicobacter sp. identified by PCR, whereas 5 of the 10 livers without tumors were positive. By use of 16S rRNA species-specific primers for H. marmotae, two additional liver samples from the nontumor group had positive PCR amplicons confirmed by Southern hybridization. A urease-, catalase-, and oxidase-positive bacterium was isolated from one liver sample from a liver tumor-positive woodchuck. By 16S rRNA analysis and biochemical and phenotypic characteristics, the organism was classified as a novel Helicobacter sp. Subsequently, four additional bacterial strains isolated from feces of cats and characterized by biochemical, phenotypic, and 16S rRNA analysis were determined to be identical to the woodchuck isolate. We propose the name Helicobacter marmotae sp. nov. for these organisms. Further studies are required to ascertain if this novel Helicobacter sp. plays a tumor promotion role in hepadnavirus-associated tumors in woodchucks or causes enterohepatic disease in cats.

Animals↗
PubMed2006

Serum antibodies to enterohepatic Helicobacter spp. in patients with chronic liver diseases and in a population with high prevalence of H. pylori infection.

BACKGROUND: Enteric Helicobacter species might be a risk factor for chronic liver and biliary tract diseases. AIMS: To analyse serum antibody levels to three enteric Helicobacter species in patients with various biliary tract and chronic liver diseases and compare results with corresponding parameters for an adult population group, known to have a high prevalence of Helicobacter pylori infection, and with healthy blood donors, to explore a possible association of enteric Helicobacter with chronic liver diseases. SUBJECTS: Sera of 90 patients with various chronic liver diseases, 121 Estonian adult persons and 68 blood donors were analysed. METHODS: Sera, previously tested for H. pylori were analysed for IgG to Helicobacter hepaticus, Helicobacter bilis and Helicobacter pullorum. ELISA was initially used for screening and exclusion of negative cases. Sera with positive ELISA results were further analysed by immunoblot. To remove cross-reactive antibodies between H. pylori and the enteric species, sera were pre-absorbed with lysed H. pylori cells. RESULTS: Liver patients showed a significantly higher seroprevalence to H. hepaticus and H. bilis, compared with the adult population group (p=0.0001 and 0.04, respectively), and to H. hepaticus, compared with blood donors (p=0.01). Patients with autoimmune hepatitis showed no significant antibody reactivity to the enteric Helicobacter spp. in contrast to patients with other chronic liver diseases. CONCLUSION: Patients with chronic liver diseases, except autoimmune hepatitis patients, showed increased antibody levels to H. bilis/H. hepaticus compared with the population and blood donors indicating a possible role of enteric Helicobacter in the natural course of chronic liver diseases. Immunoblot seems to be a promising method for serodiagnosis of infections with these fastidious pathogens.

Antibodies, Bacterial↗
PubMed2004

Detection of Helicobacter species DNA by quantitative PCR in the gastrointestinal tract of healthy individuals and of patients with inflammatory bowel disease.

In many animal species different intestinal Helicobacter species have been described and a few species are associated with intestinal infection. In humans, the only member of the Helicobacter family which is well described in literature is Helicobacter pylori. No other Helicobacter-associated diseases have definitely been shown in humans. We developed a sensitive quantitative PCR to investigate whether Helicobacter species DNA can be detected in the human gastrointestinal tract. We tested gastric biopsies (including biopsies from H. pylori positive persons), intestinal mucosal biopsies and fecal samples from healthy persons, and intestinal mucosal biopsies from patients with inflammatory bowel disease (IBD) for the presence of Helicobacter species. All gastric biopsies, positive for H. pylori by culture, were also positive in our newly developed PCR. No Helicobacter species were found in the mucosal biopsies from patients with IBD (n = 50) nor from healthy controls (n = 25). All fecal samples were negative. Our study suggests that Helicobacter species, other than H. pylori, are not present in the normal human gastrointestinal flora and our results do not support a role of Helicobacter species in IBD.

Biopsy↗
PubMed2006

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.

Animals↗