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

BACKGROUND/AIMS: The unavailability of human gastric cell lines representative of the normal gastric epithelial function such as polarized monolayer restricts the application of cell culture system in approaching the field of Helicobacter pylori (H. pylori) infected gastric mucosa models. The present investigation aimed at assessing the usefulness of NCI-N87 cell line as an adequate cellular model to study the pathophysiology of human H. pylori infection. METHODS: For the identification of epithelial phenotypes at low magnification, cells were observed on a phase-contrast microscope and confocal microscope. Transepithelial resistance (TER) was measured on NCI-N87 cells seeded on Transwell(R) to identify monolayer polarity two or three times a week after confluency. The IL-8 level was determined by ELISA at 24 hours after the administration of HP60190 and IL-1alpha on NCI-N87 cells. IL-8 level was compared in both upper and lower well with the control. RESULTS: A monolayer phenotype was observed in NCI-N87 cell lines by using confocal microscope. TER was measured as 400-500 (omega x cm2) at two or three weeks after cell culture. In NCI-N87 cell lines, IL-8 level was significantly increased after 24 hour compared to control, and was prominent in the lower well. CONCLUSIONS: These results suggest that NCI-N87 cell line may be useful in H. pylori infected gastric mucosa model.
Cell Line ; Enzyme-Linked Immunosorbent Assay ; Gastric Mucosa/*microbiology/pathology ; Helicobacter Infections/metabolism/*microbiology/pathology ; *Helicobacter pylori ; Humans ; Interleukin-8/metabolism ; Microscopy, Confocal ; Microscopy, Phase-Contrast ; Phenotype

BACKGROUND/AIMS: Oxidative stress may contribute to gastric epithelial damage and mutagenesis caused by Helicobacter pylori (H. pylori). H. pylori induces recruitment and activation of inflammatory cells, which produces reactive oxygen species. H. pylori extract directly induces the synthesis of reactive oxygen species in gastric epithelial cells and causes DNA damage. The aim of this study was to investigate the association between the levels of glutathione (GSH) and H. pylori density, histological findings, endoscopic findings, clinical variables, and virulence factors. METHODS: Gastric biopsy specimens were obtained from 73 consecutive patients. The 5,5'-dithiobis-(2-nitrobenzoic acid) reaction was used to determine GSH levels. RESULTS: The infection rate of H. pylori was 68.5%. The GSH level was not related to age, sex, alcohol intake, and endoscopic findings. The GSH level was lower in patients infected with H. pylori. GSH levels were not correlated significantly with the grades of neutrophil, intestinal metaplasia, and atrophy. However, the GSH levels were significantly correlated with H. pylori density (r=-0.296, p=0.01) and monocyte grade (r=-0.257, p=0.02). The GSH levels were not related to CagA, VacA, and UreA. CONCLUSIONS: This study suggests that H. pylori causes oxidative stresses which deplete GSH in gastric mucosa of patients infected with H. pylori.
Adolescent ; Adult ; Aged ; Female ; Gastric Mucosa/*metabolism/pathology ; Glutathione/*metabolism ; Helicobacter Infections/*metabolism/pathology ; *Helicobacter pylori ; Humans ; Male ; Middle Aged ; Oxidative Stress ; Stomach Diseases/*metabolism/microbiology/pathology

BACKGROUND/AIMS: Oxidative stress may contribute to gastric epithelial damage and mutagenesis caused by Helicobacter pylori (H. pylori). H. pylori induces recruitment and activation of inflammatory cells, which produces reactive oxygen species. H. pylori extract directly induces the synthesis of reactive oxygen species in gastric epithelial cells and causes DNA damage. The aim of this study was to investigate the association between the levels of glutathione (GSH) and H. pylori density, histological findings, endoscopic findings, clinical variables, and virulence factors. METHODS: Gastric biopsy specimens were obtained from 73 consecutive patients. The 5,5'-dithiobis-(2-nitrobenzoic acid) reaction was used to determine GSH levels. RESULTS: The infection rate of H. pylori was 68.5%. The GSH level was not related to age, sex, alcohol intake, and endoscopic findings. The GSH level was lower in patients infected with H. pylori. GSH levels were not correlated significantly with the grades of neutrophil, intestinal metaplasia, and atrophy. However, the GSH levels were significantly correlated with H. pylori density (r=-0.296, p=0.01) and monocyte grade (r=-0.257, p=0.02). The GSH levels were not related to CagA, VacA, and UreA. CONCLUSIONS: This study suggests that H. pylori causes oxidative stresses which deplete GSH in gastric mucosa of patients infected with H. pylori.
Adolescent ; Adult ; Aged ; Female ; Gastric Mucosa/*metabolism/pathology ; Glutathione/*metabolism ; Helicobacter Infections/*metabolism/pathology ; *Helicobacter pylori ; Humans ; Male ; Middle Aged ; Oxidative Stress ; Stomach Diseases/*metabolism/microbiology/pathology

OBJECTIVETo investigate the protein expression of cyclooxygenase 2 (COX-2) and nuclear factor kappa B (NF-kappaB) in gastric mucosa-associated lymphoid tissue (MALT) lymphoma and its clinical significance.

METHODSProtein expression of COX-2 and NF-kappaB in gastric MALT lymphoma were examined by immunohistochemistry of Envision two-step method. The correlations of COX-2 and NF-kappaB expression with Helicobacter pylori (Hp) infection, clinical stage, depth of tumor invasion, tumor size, recurrent rate and treatment were analyzed by univariate, multivariate and Pearson analysis.

RESULTSThe positive expression of COX-2 and NF-kappaB in gastric MALT lymphoma were 48.9%(23/47) and 36.2% (17/47) respectively, and a positive correlation was found between these two factors(r=0.326,P<0.05). Moreover, COX-2 expression was positively correlated with Hp infection,clinical stage, depth of invasion and tumor size (P<0.05). Univariate analysis showed that the overall survival of gastric MALT lymphoma patients with positive COX-2 protein (59.9 months) was shorter than that of patients with negative COX-2 protein (77.8 months), but the difference was not significant (P>0.05). The survival was significantly shorter in gastric MALT lymphoma patients with positive NF-kappaB protein (26 months) than that of patients with negative NF-kappaB protein (123.2 months)(P<0.05). Multivariate Cox regression analysis revealed that clinicopathological stage was independent prognostic factor, and associated with short survival.

CONCLUSIONUp-regulated expression of COX-2 and activation of NF-kappaB are associated with Hp infection in gastric MALT lymphoma, and their protein expression is correlated with the development of tumor and prognosis.

Cyclooxygenase 2 ; metabolism ; Female ; Gastric Mucosa ; metabolism ; microbiology ; Helicobacter Infections ; metabolism ; Helicobacter pylori ; Humans ; Lymphoma, B-Cell, Marginal Zone ; metabolism ; microbiology ; pathology ; Male ; Middle Aged ; NF-kappa B ; metabolism ; Neoplasm Staging ; Prognosis ; Stomach Neoplasms ; metabolism ; microbiology ; pathology

OBJECTIVESince application of pediatric gastroscopy in the mid-nineteen nineties, there has been a trend that the prevalence rates of pediatric gastritis and duodenal ulcer (DU) are increasing. The diagnosed rate of pediatric gastritis has accounted for 85% - 95% of the total number of children who received gastroscopy, and the rate of DU accounted for 8% - 22%. Such a high rates of the diseases may influence the development of the children severely. However, the etiology and pathogenesis of pediatric chronic gastritis and DU have not been completely elucidated. The disordered gastrointestinal hormones play a crucial role in the pediatric chronic gastritis and DU. This study focused on the expression of gastrin (GAS), somatostatin (SS) in the mucosa of gastric antrum and PCNA and Fas-L in the sinus ventriculi and their possible roles in the pathogenesis of pediatric chronic gastritis and DU.

METHODThe sinus ventriculi mucosal samples of 83 cases were collected via gastroscopic biopsy from the hospital during the recent two years and the cases were divided into five groups: group A, chronic superficial gastritis, Helicobacter pylori (Hp)(+); group B, chronic superficial gastritis, Hp(-); group C, DU, Hp(+); Group D, DU, Hp(-); Group E, normal sinus ventriculi mucosa, Hp(-). Immunohistochemical staining (En Vision) was carried out for GAS, SS, PCNA and Fas-L, and positive cells of each slide were counted (x 400). Statistically significant differences among groups for continuous data were assessed with the software SPSS10.0.

RESULTSThe expressions of GAS and SS in the groups A through E had no significant difference. The expression of PCNA in group A was significantly higher than that in group B (P < 0.05), and no significant differences were found among the other groups. There were no significant differences in expressions of Fas-L among the five groups.

CONCLUSIONThere seems to be an increasing tendency in the expressions of GAS and SS in children with chronic gastritis and duodenal ulcer. Hp infection promotes the multiplication of the sinus ventriculi mucosal epithelium cells in the pediatric chronic gastritis.

Adolescent ; Biopsy ; Child ; Child, Preschool ; Duodenal Ulcer ; metabolism ; microbiology ; pathology ; Fas Ligand Protein ; metabolism ; Female ; Gastric Mucosa ; metabolism ; pathology ; Gastrins ; metabolism ; Gastritis ; metabolism ; microbiology ; pathology ; Gastroscopy ; Helicobacter Infections ; microbiology ; Helicobacter pylori ; isolation & purification ; pathogenicity ; Humans ; Immunohistochemistry ; Intestinal Mucosa ; metabolism ; pathology ; Male ; Proliferating Cell Nuclear Antigen ; metabolism ; Pyloric Antrum ; metabolism ; pathology ; Somatostatin ; metabolism

BACKGROUND/AIMS: Peroxisome proliferator-activated receptorgamma (PPARgamma), a nuclear transcription factor, plays a critical role in the regulation of gene expression associated with inflammation and cancer. PPARgamma is expressed in human gastric cancer as well as in colon cancer. Activation of PPARgamma by ligand produces pro-apoptotic effect and ameliorate growing of cancer cells. Helicobacter pylori (H. pylori) is a main etiologic agent for gastric inflammation, and raises cell turnover in gastric epithelium. Longstanding infection with this organism is related with the development of non-cardiac gastric cancer. The aim of this study was to investigate the effect of H. pylori on the expression of PPARgamma protein and mRNA in chronic gastritis. METHODS: Gastric biopsy samples were taken from H. pylori infected (n=18) and non-infected (n=21) patients during endoscopic examination. PPARgamma expressions were assessed by real time polymerase chain reaction and immunohistochemistry. RESULTS: PPARgamma was localized to the nuclei of the foveolar epithelial cells in both infected and non-infected mucosa. PPARgamma protein expression was higher in H. pylori infected patients than in non-infected patients (3.8+/-0.4 vs. 2.6+/-1.0, H. pylori infected and non-infected, respectively; p<0.05). However, PPARgamma mRNA levels were not significantly different between the two groups (24+/-18 vs. 29+/-25, H. pylori infected and noninfected, respectively). CONCLUSIONS: PPARgamma expression is increased in the gastric mucosa of H. pylori infected chronic gastritis, which suggests a certain role of PPARgamma in the mucosal inflammatory reaction to H. pylori infection.
Adult ; Colonic Neoplasms/metabolism/microbiology/pathology ; Computer Systems ; Female ; Gastric Mucosa/*metabolism/microbiology/pathology ; Gastritis/*metabolism/microbiology/pathology ; Helicobacter Infections/*metabolism/microbiology ; *Helicobacter pylori ; Humans ; Immunohistochemistry ; Male ; Middle Aged ; PPAR gamma/*metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Stomach Neoplasms/metabolism/microbiology/pathology

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

OBJECTIVETo investigate the regulatory effect of jianpi jiedu Recipe (JJR) on the microvessel density (MVD) and cyclooxygenase-2 (COX-2) in long-term infection of Helicobacter pylori induced gastric cancer of C57BL/6 mice, thus providing experimental bases for its treatment of the H. pylori correlated gastropathy.

METHODSC57BL/6 mouse gastric cancer model induced by H. pylori infection was established by gastrogavage of H. pylori standard strain SS1. Mice were divided into the control group, the model group, low dose JJR group, and the high dose JJR group, 40 in each group. Mice were sacrificed after 72-week medication. Changes of the gastric mucosa MVD of mice in each group were detected by immunohistochemical method. Expressions of COX-2 mRNA and protein were detected by Real-time fluorescent quantitative polymerase chain reaction and immunohistochemical method.

RESULTSThe occurrence rate of gastric cancer in the control group, the model group, the low dose JJR group, and the high dose JJR group was 0, 22.2%, 11.1%, and 10.0%, respectively. The gastric mucosa MVD (number/cm2) of mice in each group was 2.50 +/- 1.54, 18.56 +/- 2.62, 14.61 +/- 3.60, and 7.39 +/- 1.75, respectively. The gastric mucosa MVD in the model group increased more obviously than that in the control group (P < 0.01). The gastric mucosa MVD significantly decreased in the low dose JJR group and the high dose JJR group (P < 0.01). Expressions of COX-2 mRNA and protein in the model group increased more obviously than those in the control group (P < 0.01). Low dose JJR and high dose JJR could decrease their expressions in a dose dependent manner.

CONCLUSIONSH. pylori infection could increase the gastric mucosa MVD of C57BL/6 mice and promote COX-2 expressions, which might play a promoting effect in the incidence of H. pylori induced gastric cancer. JJR could decrease the gastric mucosa MVD and inhibit COX-2 expressions, which might be one of its important mechanisms of preventing and treating gastric cancer.

Animals ; Cyclooxygenase 2 ; metabolism ; Drugs, Chinese Herbal ; pharmacology ; Gastric Mucosa ; blood supply ; drug effects ; metabolism ; Helicobacter Infections ; metabolism ; Helicobacter pylori ; Mice ; Mice, Inbred C57BL ; Microvessels ; pathology ; Stomach Neoplasms ; blood supply ; metabolism ; microbiology