Helicobacter pylori (H. pylori) undergoes decades long colonization of the gastric mucosa of half the population in the world to produce acute and chronic gastritis at the beginning of infection, progressing to more severe disorders, including peptic ulcer disease and gastric cancer. Prolonged carriage of H. pylori is the most crucial factor for the pathogenesis of gastric maladies. Bacterial persistence in the gastric mucosa depends on bacterial factors as well as host factors. Herein, the host and bacterial components responsible for the incipient stages of H. pylori infection are reviewed and discussed. Bacterial adhesion and adaptation is presented to explain the persistence of H. pylori colonization in the gastric mucosa, in which bacterial evasion of host defense systems and genomic diversity are included.
Gastric Mucosa/*microbiology ; Gastritis/*microbiology/pathology ; Helicobacter Infections/*microbiology ; Helicobacter pylori/*physiology ; Humans ; Stomach Neoplasms/pathology

The aim of this study was to examine whether Helicobacter pylori (H. pylori) attaches to areas of intestinal metaplasia in Korean patients. Gastric biopsy specimens with intestinal metaplasia from 8 gastric cancers, 24 gastric ulcers, 11 duodenal ulcers, and 57 chronic gastritis were examined. The specimens were stained with periodic acid-Schiff/alcian blue pH 2.5 and high-iron diamine/alcian blue pH 2.5 to identify the subtype of intestinal metaplasia, and then immunohistochemical stain was done with rabbit anti-H. pylori polyclonal antibody. In 17 patients, H. pylori attached to areas of type II intestinal metaplasia. All areas of intestinal metaplasia showing adherence contained sialomucin, and H. pylori was not detected in the areas of intestinal absorptive cells and sulfomucin-containing metaplastic cells.
Adult ; Aged ; Bacterial Adhesion/physiology* ; Female ; Gastric Mucosa/pathology* ; Gastric Mucosa/microbiology* ; Helicobacter pylori/physiology* ; Human ; Intestines/pathology* ; Intestines/microbiology* ; Korea ; Male ; Metaplasia ; Middle Age

The effect of acupuncture in the treatment of young pigs with induced enteropathogenic Escherichia coli diarrhea was histopathologically evaluated by routine hematoxylin and eosin stain. Thirty two pigs weighed 4-5kg and aged 21days old were used in this study. The animals with diarrhea were treated with traditional acupuncture, or enrofloxacin. In the group treated with traditional acupuncture, acupoint GV1 (Jiaochao) was used and in the group treated with antibiotics, enrofloxacin was injected intramuscularly. Ten pigs were inoculated with E. coli, but were not treated and served as nontreated control group. At postinoculation day 6, all pigs of the acupuncture and antibiotic treated groups recovered from diarrhea. In the ascending and descending colons of the nontreated control group, severe infiltration of inflammatory cells in the lamina propria was observed and in the fundic stomach, destruction of the fundic gland architecture and necrotic lesions were observed, however, in the same sites of the acupuncture and antibiotics treated groups, the mucosae of the colon and stomach were relatively similar to those of the normal group. These results indicate that acupuncture treatment is effective in controlling induced E. coli diarrhea in pigs at its early stage.
Acupuncture ; Animals ; Colon/cytology/microbiology/pathology ; Diarrhea/therapy/*veterinary ; Escherichia coli Infections/therapy/*veterinary ; Gastric Mucosa/cytology/microbiology/pathology ; Intestinal Mucosa/cytology/microbiology/pathology ; Male ; Stomach/cytology/microbiology/pathology ; Swine ; Swine Diseases/*microbiology/therapy

OBJECTIVETo establish a stable and reliable model of Helicobacter pylori infection in Mongolian gerbil and to observe pathological changes in gastric mucosa from the infected animals.

METHODSMongolian gerbils were randomly divided into six groups infected with H.pylori strain NCTC11637 (n=6, group N), six groups infected with H.pylori clinical strain Y06 (n=6, group Y) and six groups as negative control (n=4, group C). H.pylori suspensions at the concentrations of 2 X 10(8)CFU/ml and 2 X 10(9) CFU/ml of strain NCTC11637 and strain Y06 were prepared with Brucella broth from Columbia agar containing sheet blood. The animals in one group N and in one group Y were orally challenged once with 0.5 ml of 2 X 10(8) CFU/ml H.pylori suspension. The animals in another group N and in another group Y were orally challenged with 0.5 ml of 2 X 10(9) CFU/ml H.pylori suspension for three times at the intervals of 24 hours, respectively. The animals were killed after 2nd, 4th and 6th week of the last infection and the gastric mucosal samples were taken for urease test, bacterial isolation, routine pathological and H.pylori histochemical examinations.

RESULTSInfection rates of the animals in group N and group Y at the 2nd, 4th and 6th week after one challenge were 0%, 0%, 66.7% and 0%, 16.7%, 16.7%, respectively. Infection rates of the animals in groups N and Y at the 2nd, 4th and 6th week after three challenges were 66.7%, 100%, 100% and 66.7%, 66.7%, 100%, respectively. In animals with positive bacterial isolation H.pylori was found to colonized on the surface of gastric mucosal cells and in the gastric pits, and the lamina propria of gastric mucosal was infiltrated with chronic inflammatory cells.

CONCLUSIONBy using H.pylori suspension at high concentration of 1 X 10(9) CFU for multiple times, the orally challenged Mongolian gerbils can be prepared as a stable and reliable H.pylori infection model. H.pylori can colonize in gastric mucosa of the infected animals, and mild inflammation reactions can be seen.

Animals ; Disease Models, Animal ; Female ; Gastric Mucosa ; microbiology ; Gerbillinae ; Helicobacter Infections ; microbiology ; pathology ; Helicobacter pylori ; isolation & purification ; Immunohistochemistry

No abstract availble.
Gastric Mucosa/*metabolism/microbiology/pathology ; Gastritis/*metabolism/microbiology/pathology ; Helicobacter Infections/*metabolism/microbiology ; *Helicobacter pylori ; Humans ; PPAR gamma/*metabolism ; Predictive Value of Tests

BACKGROUND/AIMS: This study was designed to investigate the role of gastric acid in the extent of H. pylori-induced gastritis. METHODS: Twenty eight mice were innoculated with live H. pylori. They were allocated into four groups. Mice in group I received no treatment, group II mice were treated with sham injection, group III received 125microgram/kg body weight of pentagastrin, while group IV received 250microgram/kg body weight of pentagastrin subcutaneously three times a week. After 7 months, the mucosal pH, H. pylori density, neutrophils and monocytes infiltration, and the degree of atrophy were assessed in the stomach. RESULTS: In the gastric body, the densities of H. pylori were not different among groups. The degree of neutrophil infiltration was significantly lower in group IV compared to other groups (p<0.05). The degree of monocyte infiltration was also significantly lower in group IV than group III (p<0.05). In the gastric antrum, there was no significant difference of the H. pylori density, neutrophil and monocyte infiltration, and degree of atrophy among the groups. The mice with the gastric mucosal pH lower than mean of 3.2 had significant lower level of H. pylori density (1.4 vs. 2.4, p=0.04), and infiltration of neutrophils (0.9 vs. 2.3, p=0.018), and monocytes (1.2 vs. 1.8; p=0.011) than the those with mucosal pH above 3.2 in the body of stomach. CONCLUSIONS: Gastric acid plays a role in suppressing the proximal propagation of H. pylori-induced gastritis to the body of stomach.
Animals ; Female ; Gastric Acid/*metabolism ; Gastric Mucosa/pathology ; Gastritis/immunology/*microbiology ; Helicobacter Infections/*immunology/microbiology ; *Helicobacter pylori/isolation & purification ; Hydrogen-Ion Concentration ; Mice ; Mice, Inbred C57BL ; Models, Animal

No abstract availble.
Adult ; Gastric Mucosa/*pathology ; Gastritis, Hypertrophic/microbiology/*pathology ; Gastroscopy ; Helicobacter Infections/complications/*drug therapy ; *Helicobacter pylori ; Humans ; Male

BACKGROUND/AIMS: Helicobacter pylori (H. pylori) infection can lead to gastric adenoma and carcinoma through atrophic gastritis and intestinal metaplasia. Imbalance between apoptosis and proliferation may play a role in gastric carcinogenesis. We tried to investigate H. pylori infection rate, grade of gastritis, environmental risk factors, expression rate of apoptosis and cell proliferation in mucosa adjacent to tumor, and we also tried to find significant factors associated with gastric carcinogenesis. METHODS: Endoscopically diagnosed twenty cases of intestinal type gastric carcinoma, 20 cases of gastric adenoma, and 40 cases of control (normal or gastritis) were enrolled. H. pylori infection rate, histologic grading, apoptosis and immunohistochemical stain (Ki-67 and p53) to check mucosal proliferation were done in endoscopically biopsied tissues at antrum and body at least 2 cm apart from adenoma or carcinoma. RESULTS: In three groups, H. pylori infection rates were not significantly different. In the multivariate analysis, only atrophy of gland was a significant risk factor for adenoma compared to control group (OR 3.7). Intestinal metaplasia in antrum and alcohol drinking were significant risk factors for carcinoma compared to control group (OR 4.4 and 4.9 respectively). Expressions of apoptosis, Ki-67 and p53 were not significantly different in three groups. CONCLUSIONS: Intestinal metaplasia in antrum and alcohol drinking are significant risk factors for gastric carcinoma. Degree of mucosal proliferation and apoptosis in gastric mucosa adjacent to tumor are not significantly different in three groups.
Adenocarcinoma/microbiology/*pathology ; Adenoma/microbiology/*pathology ; Adult ; Aged ; Aged, 80 and over ; *Apoptosis ; *Cell Proliferation ; English Abstract ; Female ; Gastric Mucosa/*pathology ; Gastritis/microbiology/pathology ; Helicobacter Infections/complications/pathology ; Helicobacter pylori ; Humans ; Male ; Middle Aged ; Risk Factors ; Stomach Neoplasms/microbiology/*pathology

OBJECTIVE: To explore the effect of different Helicobacter pylori (H.pylori) clinical strains on the proliferation and apoptosis of gastric epithelial cells, and to observe the effect of H.pylori on gastric mucosa by Mongolian gerbil model infected H.pylori. METHODS: H.pylori isolates harvested from pathologically documented gastric carcinoma (GC, n=10) or chronic gastritis specimens (CG, n=10) were co-cultured with GES-1 cells individually. MTT assay and flow cytometry were used to determine the proliferation and apoptosis of GES-1 cells induced by H.pylori isolates. Mongolian gerbils were infected by the most (A strain) and the least (B strain) significantly proliferated H.pylori strains. Results When co-cultured with the cell/bacteria concentration ratio 1:1 and 1:50 for 12 h and the cell/bacteria concentration ratio 1:50 for 24 h, H.pylori clinical strains isolated from patients with gastric cancer promoted the proliferation of GES-1 cells, and there was significant difference in the absorbance compared with the group of gastritis strains(P<0.05). The apoptosis rate of the GC and CG groups increased significantly (P<0.05) compared with the control group when co-cultured with the cell/bacteria concentration ratio 1:50 and 1:200, and there was no significant difference between the GC group and the CG group (P>0.05). The incidences of intestinal metaplasia and dysplasia in the A strain group were significantly higher than those in the B strain group (P<0.05). CONCLUSION H.pylori strains from different disease sources have different effects on the proliferation of GES-1 cells. H.pylori isolated from gastric cancer can promote the proliferation of cells to different degrees and directly induce gastric precancerosis and gastric cancer.
Animals ; Apoptosis ; Cell Line ; Cell Proliferation ; Chronic Disease ; Gastric Mucosa ; cytology ; microbiology ; pathology ; Gastritis ; microbiology ; pathology ; Gerbillinae ; Helicobacter Infections ; pathology ; Helicobacter pylori ; pathogenicity ; Humans ; Metaplasia ; pathology ; Precancerous Conditions ; microbiology ; pathology ; Stomach Neoplasms ; microbiology ; pathology

Both lymphocytic gastritis and gastric mucosa associated lymphoid tissue (MALT) lymphoma are associated with Helicobacter pylori (H. pylori) infection. However, this association has not been fully elucidated. We report two cases of lymphocytic gastritis in 57-year-old male and 47-year-old female patients which were diagnosed after the H. pylori eradication to treat gastric MALT lymphoma. MALT lymphoma was successfully treated in case 1, but residual MALT lymphoma remained in case 2. During the follow-up endoscopic examinations, several elevated erosions in case 1 and irregular mucosal atrophy in case 2 were newly detected. Biopsy specimens showed marked infiltration of lymphocytes in the surface epithelium (56.6+/-15.9 intraepithelial lymphocytes (IELs)/100 epithelial cells in case 1 and 40.5+/-9.3 IELs/100 epithelial cells in case 2), which were exclusively CD8-positive T lymphocytes. These findings suggest that H. pylori infection may cause a monoclonal proliferation of B lymphocytes, leading to MALT lymphoma as well as polyclonal proliferation of T lymphocytes which subsequently infiltrated into the surface epithelium as a host immune reaction, resulting in lymphocytic gastritis.
Gastric Mucosa/*pathology ; Gastritis/*complications/microbiology/pathology ; Helicobacter Infections/*complications ; *Helicobacter pylori ; Humans ; Lymphocytes/*pathology ; Lymphoma, B-Cell, Marginal Zone/*complications/microbiology ; Male ; Middle Aged ; Stomach Neoplasms/*complications