Helicobacter pylori (H. pylori) has been a major concern as a gastric pathogen with unique features since discovered in the end of the 20th century. Recent data on comparative genome study have revealed that H. pylori has successfully survived with its host though over 58,000 years of evolution and migration from continent to continent. To maintain the symbiotic relationship with human, H. pylori has come up with ways to induce host tolerance as well as exert harmful injuries. Studies about H. pylori have accumulated the knowledge about how the cellular and molecular interactions are controlled and regulated to decide whether the symbiotic relationship is directed to diseases or peaceful mutualism. We reviewed recent literatures and research outcomes about the H. pylori and host interaction in molecular and cellular basis.
Adaptive Immunity ; Epithelial Cells/metabolism/microbiology/pathology ; Helicobacter Infections/immunology/metabolism/*pathology ; Helicobacter pylori/*immunology ; *Host-Pathogen Interactions ; Humans ; Symbiosis ; T-Lymphocytes/immunology/metabolism

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

OBJECTIVETo study the changes of gastric mucosal CD4(+) and CD8(+) T cells in Helicobacter pylori (Hp) infected children.

METHODSSeventy nine patients with digestive tract symptoms were assessed by endoscopy, rapid urease test and histology. Forty four patients had Hp positive chronic superficial gastritis (Hp(+)CSG) and 35 patients had Hp negative chronic superficial gastritis (Hp(-)CSG). Gastric biopsy specimens were obtained from each patient. Peripheral blood samples were obtained from 33 patients (12 with Hp(+)CSG, 21 with Hp(-)CSG). Hp infection was identified by rapid urease test and histology. Hp infection was confirmed when a patient was positive for both of these tests. Four pieces of gastric antrum mucosal specimens were placed in Hank's balanced salt solution containing 1 mmol/L dithiothreitol (DTT) and 1 mmol/L ethylenediamine tetraacetic acid (EDTA). The specimens were treated with collagenase type I (120 U/ml) for three hours at 37 degrees C with agitation. The mononuclear cells were collected by removing undigested material and washed three times with RPMI 1640. Isolated gastic mononuclear cells were stained with CD3-FITC (fluorescein isothiocyanate), CD4-PE (R-phycoerthrin), CD8-PerCP (Peridinin-chlorophyll-alpha-protein) and measured by flow cytometry. Mucosal T lymphocytes were gated for the expression of CD3. Peripheral blood lymphocyte subsets were analysed by direct immunofluorescence.

RESULTSThe percentage of isolated gastric mononuclear cells within the CD3 gate were 3.26 +/- 1.98 in Hp(-)CSG, 4.37 +/- 1.97 in Hp(+)CSG. Relative CD4(+)(%), CD8(+)(%) and CD4(+)/CD8(+) of the CD3(+) cells respectively were 23.74 +/- 10.37, 47.04 +/- 12.00, 0.52 +/- 0.23 in Hp(-)CSG group, 40.28 +/- 11.35, 27.91 +/- 8.84, 1.55 +/- 0.52 in Hp(+)CSG group. CD4(+)(%), CD4(+)/CD8(+) in Hp(+)CSG group were significantly higher than those of Hp(-)CSG group and CD8(+)(%) was lower than those of Hp(-)CSG group (P < 0.01). There were no significant differences in peripheral blood T lymphocyte subsets between the two groups.

CONCLUSIONThe difference of gastric T lymphocyte response between Hp(+)CSG and Hp(-)CSG in children indicated that the local cellular immune reaction may play a critical role in the pathogenesis of Hp infection.

Biopsy ; CD4-Positive T-Lymphocytes ; immunology ; CD8-Positive T-Lymphocytes ; immunology ; Child ; Female ; Fluorescent Antibody Technique, Direct ; Gastric Mucosa ; metabolism ; pathology ; Gastritis ; immunology ; microbiology ; pathology ; Gastroscopy ; Helicobacter Infections ; immunology ; microbiology ; pathology ; Helicobacter pylori ; immunology ; metabolism ; pathogenicity ; Humans ; Male ; Pyloric Antrum ; metabolism ; pathology ; Urease ; biosynthesis ; metabolism

OBJECTIVETo investigate whether Helicobacter pylori infection has any effects on the epithelial cell proliferation, apoptosis and P53 gene expression as well as its role in the pathogenesis of chronic gastritis.

METHODSSixty children with chronic gastritis were studied. All the children underwent upper digestive tract endoscopy and biopsy specimens were taken. Helicobacter pylori infection was determined with microscopic examination after Gimsa staining and the rapid urease test and 30 of the children were Helicobacter pylori positive and the other 30 were negative. The relation between the findings and cell proliferation was studied by immunostaining; the status of gastric apoptosis was tested by DNA fragmentation in situ using TdT-mediated dUTP biotin nick end labeling (TUNEL). Immunohistochemical method was used to detect the expression of P53 protein; CagA antibody was tested by Western blotting.

RESULTS(1) The proliferative index and apoptosis index in children with Helicobacter pylori infection with CagA positive gastritis were much higher than those of Helicobacter pylori negative gastritis patients [(11.56 +/- 4.21)% vs. (5.85 +/- 2.21)%, (10.58 +/- 5.31)% vs. (2.86 +/- 0.64)%, P < 0.01]. (2) The proliferative index and apoptosis index in 30 cases with Helicobacter pylori infection with CagA positive gastribis were much higher than 21 cases who were cured by effective drugs [(11.50 +/- 4.11)% vs. (3.74 +/- 2.30)%; (10.58 +/- 4.02)% vs. (3.74 +/- 2.30)%, P < 0.01]. (3) The expression of P53 protein in Helicobacter pylori with CagA positive gastritis children was much higher than that of Helicobacter pylori negative cases [(63% vs 16%), P < 0.1].

CONCLUSIONCagA positive Helicobacter pylori infection with gastritis improved gastric epithelial cell proliferation and apoptosis. The abnormal expression of P53 protein in gastric epithelium may play an important role in regulation of the processes.

Antibodies, Bacterial ; blood ; Antigens, Bacterial ; immunology ; Apoptosis ; Bacterial Proteins ; immunology ; Biopsy ; Cell Proliferation ; Child ; Child, Preschool ; Epithelial Cells ; metabolism ; Female ; Gastric Mucosa ; pathology ; Gastritis ; complications ; pathology ; Helicobacter Infections ; complications ; pathology ; Helicobacter pylori ; Humans ; In Situ Nick-End Labeling ; Male ; Tumor Suppressor Protein p53 ; metabolism

We tested correlations between anti-Helicobacter pylori IgG and IgA levels and the urease test, anti-CagA protein antibody, degree of gastritis, and age. In total, 509 children (0-15 years) were enrolled. Subjects were stratified as 0-4 years (n = 132), 5-9 years (n = 274), and 10-15 years (n = 103) and subjected to the urease test, histopathology, ELISA, and western blot using whole-cell lysates of H. pylori strain 51. The positivity rate in the urease test (P = 0.003), the degree of chronic gastritis (P = 0.021), and H. pylori infiltration (P < 0.001) increased with age. The median titer for anti-H. pylori IgG was 732.5 IU/mL at 0-4 years, 689.0 IU/mL at 5-9 years, and 966.0 IU/mL at 10-15 years (P < 0.001); the median titer for anti-H. pylori IgA was 61.0 IU/mL at 0-4 years, 63.5 IU/mL at 5-9 years, and 75.0 IU/mL at 10-15 years (P < 0.001). The CagA-positivity rate was 26.5% at 0-4 years, 36.5% at 5-9 years, and 46.6% at 10-15 years for IgG (P = 0.036), and 11.3% at 0-4 years, 18.6% at 5-9 years, and 23.3% at 10-15 years for IgA (P < 0.001). Anti-H. pylori IgG and IgA titers increased with the urease test grade, chronic gastritis degree, active gastritis, and H. pylori infiltration. Presence of CagA-positivity is well correlated with a high urease test grade and high anti-H. pylori IgG/IgA levels.
Adolescent ; Antibodies, Bacterial/*blood ; Antigens, Bacterial/*analysis/immunology ; Bacterial Proteins/*analysis/immunology/metabolism ; Blotting, Western ; Child ; Child, Preschool ; Chronic Disease ; Enzyme-Linked Immunosorbent Assay ; Female ; Gastritis/pathology ; Helicobacter Infections/blood/microbiology/*pathology ; Helicobacter pylori/isolation & purification/*metabolism ; Humans ; Immunoglobulin A/*blood ; Immunoglobulin G/*blood ; Infant ; Infant, Newborn ; Male ; Severity of Illness Index ; Urease/metabolism

OBJECTIVETo determine the influence of Helicobacter pylori (H. pylori) on gastric cancer-related antigen MG7 expression.

METHODSThe H. pylori infection and the expression level of antigen MG7 in gastric mucosa were determined by HE stain, PCR, ELISA and immunohistochemistry in 291 patients with H. pylori-related conditions, among whom 34 were followed-up.

RESULTSNo significant difference was found between H. pylori-negative and H. pylori-positive intestinal metaplasia, atrophic gastritis and dysplasia of gastric epithelium in positive rate of antigen MG7 expression. There was significant difference between H. pylori-negative and H. pylori-positive superficial gastritis in the positive rate of MG7 expression (P < 0.05). During follow-up, one of 3 H. pylori-negative cases turned to be H. pylori-positive, and its MG7 expression turned to be higher at the same time. Three of 31 H. pylori-positive patients were discovered as having early gastric cancer, among whom one with antigen MG7 expression (+ + +) was found to have a reduced Mg7 expression accompanied with H. pylori eliminutied after operation.

CONCLUSIONThere is correlationship between H. pylori infection and MG7 expression in superficial gastritis. Although the MG7-positive lesions with H. pylori infection shows a benign nature in morphology, they also have the potential risk of developing into gastric cancer. Therefore, they should be followed up, during which special attention should be paid to patients with increased MG7 expression.

Antibodies, Bacterial ; blood ; Antigens, Neoplasm ; biosynthesis ; DNA, Bacterial ; genetics ; Enzyme-Linked Immunosorbent Assay ; Gastric Mucosa ; metabolism ; microbiology ; pathology ; Gastritis ; metabolism ; microbiology ; Helicobacter Infections ; metabolism ; microbiology ; Helicobacter pylori ; genetics ; growth & development ; immunology ; Humans ; Immunohistochemistry ; Polymerase Chain Reaction ; Stomach Diseases ; metabolism ; microbiology ; Stomach Ulcer ; metabolism ; microbiology