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PubMed2005

[Perspective of Helicobacter pylori research: molecular pathogenesis of Helicobacter pylori virulence factors].

Helicobacter pylori (H. pylori) causes chronic gastritis in human stomach, a minority of which progress to peptic ulcer disease, atrophic gastritis, or gastric malignancies. Clinical outcomes of H. pylori infection has been shown to depend on the variability of H. pylori virulence factors, host susceptibility, environmental factors and their interactions. This review provides an update on the molecular pathogenesis of H. pylori infection, focused on H. pylori virulence factors, H. pylori-gastric epithelium interactions, and modulation of host cell signaling. Understanding of H. pylori molecular pathogenic mechanism will facilitate the development of novel treatment strategies for eradication of the bacterium and prevention of H. pylori-induced gastropathy.

Helicobacter Infections↗
PubMed2006

[Influence of resistance of Helicobacter pylori to antibiotics on the Helicobacter pylori eradication regimens].

OBJECTIVE: To investigate the influence of resistance of Helicobacter pylori (H. pylori) to antibiotics on the efficacy of lansoprazole triple therapy for H. pylori eradication. METHODS: 157 patients, 102 males and 55 females, aged 42.7 (18 - 70), with upper abdominal symptoms, 59 with chronic gastritis and 98 with peptic ulcer, underwent gastroendoscopy 157 H. pylori strains were isolated from the gastric biopsy specimens of these patients and cultured. Minimal inhibitory concentrations of 3 antibiotics (metronidazole and clarithromycin) were determined by E-test. The 157 patients were treated by triple therapies, including lansoprazole, metronidazole, and clarithromycin for 7 days. Reexamination was done at least 4 weeks after the therapy. RESULTS: The resistance rates of H. pylori to metronidazole and clarithromycin were 45.9% (72/157) and 18.5% (29/157) respectively. The reexamination showed an eradication rate of H. pylori of 61.8% (97/157). The eradication rates of the metronidazole-sensitive and resistant strains were 89.4% (76/85) and 29.2% (21/72) respectively (P < 0.01), and the eradication rates of the clarithromycin-sensitive and resistant strains were 72.7% (93/128) and 16.0% (4/29) respectively (P < 0.01). Presence of a gastroduodenal ulcer, age and gender did not differ significantly between the eradicated and non-eradicated groups (all P > 0.05). CONCLUSION: Resistance of H. pylori to antibiotics is the most important cause of the failure of H. pylori eradication.

Adolescent↗
PubMed1993

[Availability of determination of serum anti-Helicobacter pylori IgG antibody in diagnosis of Helicobacter pylori infection].

We studied on clinical availability of determination of serum anti-Helicobacter pylori (HP) IgG antibody in diagnosis of HP infection compared with bacterial culture. The population of this study consisted of patients who underwent endoscopic examination in our hospital. Detection and quantification of HP were made by the culture of biopsy specimens taken from the antrum and the body of the stomach. And, simultaneously, serum anti-HP antibody (HP-Ab) was measured by ELISA. The levels of HP-Ab in culture positive patients, 40.6 +/- 33.7U, are significantly higher than that of culture negative patients, 10.6 +/- 9.1U. Sensitivity and specificity in diagnosis of HP infection using determination of serum HP-Ab were 96.2% and 60.0% respectively. Significant correlation was found between the levels of serum HP-Ab and the amounts of HP bacilli in the biopsy specimen taken from body of the stomach.

Aged↗
PubMed1996

[Triple ranitidine therapy in Helicobacter pylori infection. Recommendation for effective, safe and cost effective combination for Helicobacter pylori eradication].

Peptic ulcer disease induced by infection with Helicobacter pylori can be cured by eradicating the organism. In the meantime, such eradication therapy has moved beyond the experimental stage and can now be applied in the doctor's office, effectively, safely and inexpensively. A seven to twelve day course of treatment comprising a gastric acid inhibitor (20 mg omeprazole twice daily is no more effective than 300 mg ranitidine daily), 500 mg metronidazole twice daily, and 1 g amoxicillin twice daily results in an eradication rate of about 90%. That is, repeat treatment is needed in only one in ten patients. The cost of eradication therapy, however, varies considerably: the treatment recommended by the "initiative in support of the new form of ulcer treatment" costs DM 512.27, while equally effective treatment using generics costs only about one-fifth of this amount. In this way, a troublesome illness that for thousands of years has received only symptomatic treatment and whose sequelae cause high costs can now be treated causally with a high success rate and also a favourable cost-benefit ratio.

Amoxicillin↗
PubMed1997

Body-fundic gastric ulcer and Helicobacter pylori: muco-peptic cells expansion (immature cells) in Helicobacter pylori positive patients.

It is generally agreed that Helicobacter pylori (Hp) plays a key role in alterating regulatory factors affecting cellular proliferation during the disease process. During chronic superficial gastritis there is, in case of moderate/severe activity, a foveolar-superficial expansion of immature muco-peptic cells. In the present experience this phenomenon has been evaluated in the surrounding areas of 22 body-fundic gastric ulcer (BFGU). The 72.7% of BFGU were Hp positive. The expansion was detectable in 68.7% of Hp positive BFGU. The expansion process involves the substitution of mature cells with immature one determining a reduction of the efficacy of the mucosa barrier in association with an increment of aggressive factors (mucosal pepsins). This phenomenon in relation with host genetic susceptibility may favor peptic ulcer.

Cell Division↗
PubMed2004

Proteomic analysis of a ferric uptake regulator mutant of Helicobacter pylori: regulation of Helicobacter pylori gene expression by ferric uptake regulator and iron.

The ferric uptake regulator (Fur) protein is a Fe(2+)-dependent transcriptional repressor that binds to the Fur-box of bacterial promoters and down-regulates gene expression. In this study, to investigate global gene regulation by Fur in response to iron in Helicobacter pylori, a causative agent of human gastric diseases, we compared the proteome profiles of the H. pylori strain 26695 and its isogenic fur mutant grown under iron-rich and iron-depleted conditions. In total, 93 protein spots were found to be up- or down-regulated by more than 2-fold by either a fur mutation or iron-depletion. From these, 39 spots were identified by matrix-assisted laser desorption/ionization time of flight analysis to be 29 different proteins of diverse functions, including energy metabolism, transcription and translation, detoxification, biosynthesis of amino acids and nucleotides and production of the cell envelope. Expression of six proteins was found to be higher in the fur mutant than in the wild-type bacteria, indicating Fur-mediated repression. Eleven proteins were activated by Fur; five responded to iron and the others were not iron-responsive. The remaining 12 proteins were not under Fur-regulation but responded to iron in a positive or negative manner. Seven different types of gene regulation via Fur and iron were identified. These findings demonstrate that the H. pylori Fur protein functions as a classical transcriptional repressor but can also function as an activator, providing evidence for the presence of Fur-mediated positive regulation in H. pylori.

Bacterial Proteins↗
PubMed2001

Helicobacter infection and phospholipase A2 enzymes: effect of Helicobacter felis-infection on the expression and activity of sPLA2 enzymes in mouse stomach.

The murine gastric mucosa possesses very high secretory type phospholipase A2 activity. Northern and Western blots indicated that the pancreatic-type, sPLA2-IB represents the predominant form of sPLA2 enzymes present in the gastric mucosa. Both sPLA2-IB mRNA and protein in the gastric mucosa exceeded levels found in the pancreas, and in contrast to the pancreatic enzyme it was present primarily in the active state. The sPLA2-IB gene is not expressed in the murine small intestine and colon. Infection by the gastritis-inducing bacteria, Helicobacterfelis (H. felis) dramatically and time dependently decreased the PLA2 activity in the glandular stomach of the mouse strain, C57BL/6, sensitive to the organism, which appeared to be related to a decrease in the percentage of sPLA2-IB present in the active form. This bacterial-induced reduction in PLA2 activity was not observed in BALB/c mice that fail to develop gastritis in response to H. felis infection. C57BL/6 mice do not, while BALB/c mice express, the PLA2-II enzyme. The H. felis-induced reduction in sPLA2-IB activity may weaken the gastric barrier by reducing the local concentration of arachidonic and linoleic acid, liberated from membrane phospholipids, the major precursors of 'cytoprotective' prostaglandins. Data presented here suggest that both sPLA2-IB and sPLA2-II enzymes may contribute to the gastric response to Helicobacter infection.

Animals↗
PubMed1997

Helicobacter pylori and non-Helicobacter pylori bacterial flora in gastric mucosal and tumour specimens of patients with primary gastric lymphoma.

There is an association between Helicobacter pylori (H. pylori) and gastric mucosa-associated lymphoid tissue (MALT) and MALT lymphoma. Histologically, mainly non-specific stains are used to detect H. pylori, such as haematoxylin-eosin (HE) or modified Giemsa (MG). In this study, both a MG and a specific immunohistochemical stain (IMM) for H. pylori (Dako B471) were performed on sequential slides of resected material containing tumour and non-tumorous gastric mucosa from patients with primary gastric lymphoma (n = 52). Special attention was paid to the presence of non-H. pylori bacterial flora diagnosed by a positive MG (according to form and localization) and a subsequently negative IMM. On all slides, bacterial density was scored semiquantitatively (grades 0, 1, 2, 3). In total, 32 (61.5%) patients were H. pylori positive using IMM and 34 (65.4%) were non-H. pylori positive using MG. In 24 out of the 34 patients, the non-H. pylori flora consisted mainly of cocci in combination with rods in 15 patients, mostly in minor quantities; in another 10 patients, high numbers of both cocci and different types of rods were present. Most non-H. pylori bacteria were localized superficially, although in 22 patients minor quantities of non-H. pylori were also seen in the glandular lumina. After all of the patients had been analysed, no differences in the density of H. pylori and of non-H. pylori flora were found. Only when comparing patients who had a small-cell lymphoma with those who had a large-cell lymphoma was a significantly higher density of H. pylori found in the corpus mucosa of large-cell lymphomas and a higher prevalence of non-H. pylori was found in tumours, in antrum or corpus, of patients with large-cell lymphomas. In conclusion, with joint evaluation using MG and a H. pylori-specific immunohistochemical stains, the proportion of H. pylori-positive gastric lymphoma patients was lower than in most previous studies but other bacteria were found in a relatively high proportion. The role of the non-H. pylori intragastric bacterial flora identified in this study has to be further elucidated in the aetiopathogenesis of primary gastric lymphoma.

Adult↗
PubMed1997

Construction of a Helicobacter pylori-Escherichia coli shuttle vector for gene transfer in Helicobacter pylori.

In this study, a Helicobacter pylori-Escherichia coli shuttle vector was constructed for transferring DNA into H. pylori. The smallest cryptic plasmid (1.2 kb), pHP489, among those harbored by 77 H. pylori isolates was selected as a base replicon for constructing vectors. HindIII-digested pHP489 was ligated with a kanamycin resistance gene [aph(3')-III], which originated from Campylobacter jejuni, to produce the recombinant plasmid pHP489K. pHP489K was efficiently transformed into and stably maintained in H. pylori strains. The shuttle vector pBHP489K (3.6 kb) was constructed by the recombination of pHP489, ColE1, and aph(3')-III sequences. pBHP489K was reciprocally transformed into and maintained in both H. pylori and E. coli. Introduction of the shuttle vector clone DNA (pBHP489K/AB; 6.7 kb), containing the ureA and ureB genes of H. pylori, into urease-negative mutants of H. pylori led to the restoration of their urease activity. The transformants were confirmed to contain the incoming plasmid DNA. pBHP489K satisfied the requirements for an H. pylori-E. coli shuttle vector, implying that it might be a useful vector for investigating pathogenicity and restriction-modification systems of H. pylori.

Cloning, Molecular↗
PubMed2001

Helicobacter pylori from asymptomatic hosts expressing heptoglycan but lacking Lewis O-chains: Lewis blood-group O-chains may play a role in Helicobacter pylori induced pathology.

Helicobacter pylori is a widespread Gram-negative bacterium responsible for the onset of various gastric pathologies and cancers in humans. A familiar trait of H. pylori is the production of cell-surface lipopolysaccharides (LPSs; O-chain --> core --> lipid A) with O-chain structures analogous to some mammalian histo-blood-group antigens, those being the Lewis determinants (Lea, Leb, Lex, sialyl Lex, Ley) and blood groups A and linear B. Some of these LPS antigens have been implicated as autoimmune, adhesion, and colonization components of H. pylori pathogenic mechanisms. This article describes the chemical structures of LPSs from H. pylori isolated from subjects with no overt signs of disease. Experimental data from chemical- and spectroscopic-based studies unanimously showed that these H. pylori manufactured extended heptoglycans composed of 2- and 3-linked D-glycero-alpha-D-manno-heptopyranose units and did not express any blood-group O-antigen chains. The fact that another H. pylori isolate with a similar LPS structure was shown to be capable of colonizing mice indicates that H. pylori histo-blood-group structures are not an absolute prerequisite for colonization in the murine model also. The absence of O-chains with histo-blood groups may cause H. pylori to become inept in exciting an immune response. Additionally, the presence of elongated heptoglycans may impede exposure of disease-causing outer-membrane antigens. These factors may render such H. pylori incapable of creating exogenous contacts essential for pathogenesis of severe gastroduodenal diseases and suggest that histo-blood groups in the LPS may indeed play a role in inducing a more severe H. pylori pathology.

Carbohydrate Sequence↗
PubMed2006

[Effects of Helicobacter pylori and Helicobacter pylori-related cytokines on apoptosis of gastric epithelial cells and mechanisms thereof].

OBJECTIVE: To investigate the influence of Helicobacter pylori (H. pylori) and H. pylori-related cytokines on the apoptosis of gastric epithelial cells and mechanisms thereof. METHODS: (1) Human gastric cancer cells of the line AGS and human gastric epithelial cells of the line GES-1 were cultured as control group, or incubated with H. pylori alone or H. pylori in combination with exogenous cytokines: interleukin (IL)-1beta, IL-8, or IL-10 for 24 hours. Then flow cytometry (FCM) was used to determine the rate of apoptosis. (2) The GES-1 and AGS cells were incubated with H. pylori for 24 hours and exogenous cytokines for 2 hours respectively. Then RT-PCR was used to examine the level of Fas mRNA expression. (3) Another GES-1 and AGS cells were cultured as control group, or incubated with FasL alone or FasL + exogenous cytokine for 2 hours (incubated with IL-1beta, IL-8, or IL-10 for 2 hours before being added with FasL). Then FCM was used to detect the apoptosis rate. RESULTS: (1) In comparison to the apoptosis level of control group, H. pylori induced an increase in the apoptosis rate of GES-1 and AGS cells by 113.0% and 47.0% respectively (both P < 0.05). The H. pylori-induced apoptosis rates of GES-1 cells (by 29.6% or 25.8%) and AGS cells (by 19.7% or 21.1%) were reduced by IL-1beta or IL-10 (all P < 0.05). IL-8 increased the H. pylori-induced apoptosis level of GES-1 cells by 19.9% (P < 0.05). (2) In the baseline status, both GES-1 and AGS cells showed Fas mRNA expression. The Fas mRNA expressions of the GES-1 and AGS cells incubated with H. pylori were increased by 89.0% and 36.0% respectively (both P < 0.05) in comparison to that of the control group. IL-1beta and IL-10 had no significant effect on the basal Fas mRNA expressions in both GES-1 and AGS cells (all P > 0.05). IL-8 up-regulated the basal Fas mRNA expression level of the GES-1 cells by 33.0% (P < 0.05). (3) IL-1beta and IL-10 inhibited the FasL-induced apoptosis rate of the GES-1 cells (by 30.3% and 32.5% respectively) and AGS cells (by 44.2% and 51.5% respectively) (all P < 0.05). IL-8 enhanced the FasL-induced apoptosis level of the GES-1 cells by 100% (P < 0.05). CONCLUSION: The gastric epithelium apoptosis induced by H. pylori may be in association with Fas receptor. IL-8 may enhance the H. pylori-induced apoptosis by up-regulating the Fas receptor expression. IL-1beta and IL-10 may modulate the apoptosis through other mechanisms.

Apoptosis↗
PubMed1991

A topographical relationship between Helicobacter pylori and gastritis: quantitative assessment of Helicobacter pylori in the gastric mucosa.

A topographical relationship between the number of Helicobacter pylori in the gastric mucosa and the histological severity of gastritis was studied in 902 pairs of biopsy specimens taken from 314 patients. A pair of biopsies were taken from the antrum, the lesser curvature of the middle body, and the greater curvature of the upper body of the stomach. The quantitative assessment of H. pylori was made based on smear, culture, and tissue section. The histological severity of gastritis was assessed as to the degrees of mononuclear cell and polymorphonuclear leukocyte infiltration. A positive correlation was confirmed between the number of H. pylori and the severity of polymorphonuclear leukocyte infiltration. The degrees of inflammatory cells infiltration in the specimens with H. pylori colonization were significantly lower in the upper body than in the antrum.

Adolescent↗
PubMed1997

Specific detection of Helicobacter pylori and non-Helicobacter pylori flora in small- and large-cell primary gastric B-cell non-Hodgkin's lymphoma.

BACKGROUND: Primary gastric non-Hodgkin's lymphomas possibly develop in response to local infection by Helicobacter pylori (H. pylori). We investigated the presence of H. pylori and non-H. pylori flora histologically in small- and large-cell primary gastric lymphoma using a specific staining method. MATERIALS AND METHODS: Specimens of 52 cases of primary gastric lymphoma (17 small cell, 35 large cell) were stained with modified Giemsa (MG) and immunohistochemically using a polyclonal antibody against H. pylori (IHC). RESULTS: Thirty-two cases (61.5%) (small cell 76% versus large cell 53%, P > 0.05) showed immunoreactivity for H. pylori in the mucosa surrounding the tumor. Remarkably, there was localization of H. pylori in the neck of the gastric glands in 3 cases. Non-H. pylori flora was seen in 35 cases (76.3%) (small cell 53% versus large cell 74%, P > 0.05). In 20 cases, this non-H. pylori flora was mixed with H. pylori. Five cases showed no bacterial flora at all. CONCLUSIONS: (1) Using immunohistochemistry, the prevalence of gastric lymphoma cases with H. pylori (61.5%) approximates that of H. pylori in the normal population. (2) No statistical difference was found between the occurrence of H. pylori and non-H. pylori bacterial flora in small- versus large-cell lymphoma. (3) Our results suggest that H. pylori may not be the only etiologic factor in primary gastric lymphoma.

Female↗