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 evaluate the presence of Helicobacter (H.) spp. in swine affected by gastric ulceration. Stomachs from 400 regularly slaughtered swine were subjected to gross pathological examination to evaluate the presence of gastric ulcers. Sixty-five samples collected from ulcerated pars esophagea and 15 samples from non-ulcerated pyloric portions were submitted to histopathological and molecular analyses, to detect Helicobacter spp., H. suis and H. pylori by PCR. Feces and saliva swabs were also collected from 25 animals in order to detect in vivo the presence of Helicobacter spp.. Gastric ulcers were detected in 373 cases (93%). The presence of ulcers in association with inflammatory processes was further confirmed by histological examination. Forty-nine percent (32/65) of the ulcerated esophageal portions as well as 53% (8/15) of the non-ulcerated pyloric portions were positive for Helicobacter spp. by PCR. The Helicobacter spp. positive samples were also positive for H. suis, while H. pylori was not detected. These results were confirmed by restriction enzyme analysis. With regard to feces and saliva samples, 15/25 (60%) and 16/25 (64%) were positive for Helicobacter spp. PCR, respectively but all were negative in H. suis and H. pylori specific PCR.
Animals ; Feces/*microbiology ; Helicobacter/*isolation & purification ; Polymerase Chain Reaction/veterinary ; Restriction Mapping/veterinary ; Saliva/*microbiology ; Stomach/*microbiology ; Stomach Ulcer/microbiology/pathology/*veterinary ; Swine ; Swine Diseases/*microbiology/pathology

Stomach is the most common site of primary extranodal lymphoma. Mucosa-associated lymphoid tissue (MALT) lymphoma is a unique type of extranodal lymphoma which is associated with Helicobacter pylori (H. pylori). The development of low-grade MALT lymphoma of stomach is dependent on H. pylori. A transformed clone carrying the translocation t(11;18)(q21;q21) forms a MALT lymphoma, the growth of which is independent of H. pylori and will not respond to bacterial eradication. And inactivation of the tumor suppressor genes, p53 can lead to high-grade transformation. Endoscopic ultrasound (EUS) is essential to document the extent of disease and is superior to CT scan in the detection of spread to perigastric lymph nodes and follow-up EUS may determine the response to therapy and detect the relapse in early phase. Lesions that are confined to the mucosa or submucosa of gastric wall can be successfully treated with H. pylori eradication. Those low-grade MALT lymphomas that are not H. pylori positive or do not respond to antibiotic therapy can be treated with surgery, radiation, or chemotherapy. Follow-up is critical in all patients who have been treated with H. pylori eradication and consists of multiple endoscopic biopsies and EUS.
Helicobacter Infections/complications ; Helicobacter pylori ; Humans ; *Lymphoma, B-Cell, Marginal Zone/microbiology/pathology ; Stomach Diseases/complications ; *Stomach Neoplasms/microbiology/pathology

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

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

BACKGROUND: Helicobacter pylori (H. pylori) has been considered a definitive carcinogen in gastric cancer. Telomerase is activated in gastric cancer and some premalignant gastric lesions, including intestinal metaplasia (IM). In this study, we evaluated the relationships of both H. pylori infection and telomerase activity with endoscopic and histologic features in IM. The effects of H. pylori eradication on endoscopic, histologic and biochemical changes were evaluated. METHODS: Endoscopic biopsies were obtained from 43 patients with IM for rapid urease, histologic and telomerase tests. The endoscopic and histologic features, H. pylori infection and telomerase were assessed. After H. pylori eradication, 15 patients were re-evaluated and compared after 4 months. RESULTS: Thirty-four (79.1%) patients were infected with H. pylori. The incidence of H. pylori infection was borderline correlated to the severity of IM (p=0.076). Telomerase was elevated in eight (18.6%) patients. Telomerase tends to be high in subtype III and endoscopic grade III of IM. After H. pylori eradication, endoscopic extent (p=0.039) and histologic severity (p=0.074) showed improvements, and telomerase decreased significantly (p=0.0001). CONCLUSION: Our data suggest that telomerase is associated with the severity and extent of IM and that H. pylori eradication improves the endoscopic and histologic features in IM, and decreases telomerase activity. H. pylori eradication can be considered one of the methods to prevent gastric cancer in patients with H. pylori-infected IM. Further long-term and large-scaled study will be needed.
Female ; Helicobacter Infections/*enzymology ; *Helicobacter pylori ; Human ; Intestinal Mucosa/enzymology/microbiology/*pathology ; Male ; Metaplasia/enzymology/microbiology ; Middle Aged ; Precancerous Conditions/enzymology/microbiology ; Stomach Neoplasms/*enzymology/microbiology ; Telomerase/*metabolism

OBJECTIVE: To explore the relationship between the Helicobacter pylori (H.pylori) infection and gastric mucosa change and blood-lipid in people undergoing the physical examination in Changsha. METHODS: A total of 2 264 people undergoing physical examination were divided into an H. pyloripositive group (n=1 068) and an H. pylori-negative group (n=1 196). Gastric mucosa change was diagnosed by gastroscopy, blood-lipid and blood sugar were detected, and the statistical analysis was performed. RESULTS: The incidence rate of H.pylori infection was 47.2%. The incidence rate of gastric mucosal erosion, gastric ulcer, duodenal ulcer, gastric mucosal atrophy, gastric polyp, dyslipidemia, increase of triglyceride were (TG) and decrease of the high density lipoprotein cholesterol (HDL-C) in the H.pylori-positive group were all higher than those in the H.pylori-negative group (P<0.01 or P<0.05). In the H. pylori-positive group, the level of TG in people with gastric mucosal erosion, gastric ulcer and duodenal ulcer was higher than that in people with normal gastric mucosa or mild gastritis, and HDL-C was lower than that in people with normal gastric mucosa or mild gastritis. CONCLUSION H. pylori infection can induce the gastric mucosa injury and dyslipidemia, which may result in the occurrence and development of coronary heart disease by increasing TG and decreasing HDL-C, thus increasing the risk of atherosclerosis.
Adenomatous Polyps ; Cholesterol, HDL ; blood ; Duodenal Ulcer ; microbiology ; physiopathology ; Dyslipidemias ; microbiology ; Gastric Mucosa ; microbiology ; pathology ; Gastritis ; microbiology ; physiopathology ; Helicobacter Infections ; physiopathology ; Helicobacter pylori ; Humans ; Lipids ; blood ; Physical Examination ; Stomach Neoplasms ; Stomach Ulcer ; microbiology ; physiopathology ; Triglycerides ; blood

The occurrence of Helicobacter pylori(H.pylori) and its relationship with gastric mucosa were studied by light and electron microscopy and culture of biopsy specimens from gastric mucosa of 160 patients with upper gastrointestinal symptoms. H. pylori were present in 96.6% of patients with active chronic gastritis, 100% of patients with duodenal ulcer and 76.9% of patients with gastric ulcer, while present in only 6.3% of individuals with histologically normal gastric mucosa. The bacteria colonized the antral mucosa more frequently than the body or than the duodenal cap mucosa. The bacteria were rarely seen in the intestinalized epithelium per se, but there was no significant difference in prevalence of H. pylori between gastritis with intestinal metaplasia and gastritis without intestinal metaplasia. H. pylori could be seen in close association with the surface of gastric epithelial cells below the mucus layer without evidence of intracellular parasitism, All of the strains tested were susceptible to penicillin, erythromycin, and most of them susceptible to tinidazole and bismuth salts. It is concluded that H. pylori are highly associated with gastritis and peptic ulcer diseases and its prevalence rates in patients with those diseases is higher than in developed countries. This strong association of H. pylori infection with gastritis and peptic ulcer diseases suggest a possible etiologic role for the bacterium in those diseases.
Adolescent ; Adult ; Aged ; Chronic Disease ; Duodenal Ulcer/*microbiology/pathology ; Female ; Gastric Mucosa/microbiology/pathology/ultrastructure ; Gastritis/*microbiology/pathology ; *Helicobacter Infections ; Helicobacter pylori/*isolation & purification ; Human ; Male ; Middle Aged ; Prospective Studies ; Stomach Ulcer/*microbiology/pathology ; Support, Non-U.S. Gov't

No abstract available.
Adult ; Duodenal Diseases/*diagnosis/microbiology/pathology ; Gastric Mucosa/microbiology/pathology ; Gastroscopy ; Humans ; Male ; Stomach Diseases/*diagnosis/microbiology/pathology ; Syphilis/*diagnosis/microbiology/pathology ; Tomography, X-Ray Computed ; Treponema pallidum/isolation & purification