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

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

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

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

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 Mucosa-associated lymphoid tissue (MALT) lymphoma, which was first described in 1983, is known to be caused by chronic Helicobacter pylori (HP) infection, which triggers lymphoid infiltration and formation of organized lymphoid tissue. In approximately two thirds of cases of MALT, the lymphoma has been observed to regress after treatment of H. pylori infection; this provides strong evidence of a causative role of HP in the etiology of MALT. We report a case of a 67-year-old female patient with a high-grade MALT lymphoma of the liver; this occurred six years after complete remission of a low-grade gastric MALT lymphoma and after complete eradication of H. pylori. there was no recurrence of the previous low-grade gastric MALT lymphoma. Based on radiological and pathologic findings, the high-grade MALT was considered to result from transformation of the low-grade gastric MALT lymphoma.
Stomach Neoplasms/*pathology ; Lymphoma, Mucosa-Associated Lymphoid Tissue/microbiology/*pathology ; Liver Neoplasms/microbiology/*secondary ; Humans ; Helicobacter pylori/isolation & purification ; Female ; Fatal Outcome ; Aged

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

OBJECTIVE: To observe the changes of cell gap junction ultrastructure of gastric epithelial cells in patients with gastric cancer(GC) and precancerous lesion(PL),and to investigate the relation between these changes and H.pylori infection. METHODS: Seventy patients with GC, 88 with PL, and 33 with chronic superfial gastritis (CSG) were studied. H.pylori was detected by rapid urease test,basic fuchsin stain and 14C-urea breath test. The CagA gene of H.pylori was determined by polymerase chain reaction(PCR).The cell gap junction ultrastructure was observed under transmission electronic microscope. RESULTS: Length of junction/unit perimeter of gastric epithelial cells in patients with PL was smaller than that in CSG patients, and the smallest width of the intercellular space was bigger than that in CSG patients. The number of cell junction, the number of junction/unit perimeter, and the length of junction/unit perimeter in patients with GC were all smaller than those in patients with CSG or PL, and its smallest width of the intercellular space was bigger than that in patients with CSG. In patients with GC, the number of cell junction, the number of junction/unit perimeter and the length of junction/unit perimeter in CagA+ H.pylori group were smaller than those in CagA(-) H.pylori group, and its smallest width of the intercellular space was bigger than that in CagA(-) H.pylori group. In PL patients, the intercellular space decreased, and the length of cell junction of gastric epithelial cells became bigger after H.pylori eradication. The length of junction/unit perimeter in patients of H.pylori eradication was bigger than that in patients without eradication, and the smallest width of the intercellular space was smaller than that in patients without eradication. CONCLUSION The changes of cell gap junction of gastric epithelial cells in patients with GC and PL are associated with H.pylori infection especially CagA+ H.pylori infection. Eradication of H.pylori can promote the formation of cell junction.
Adenocarcinoma ; microbiology ; ultrastructure ; Epithelial Cells ; ultrastructure ; Female ; Gastric Mucosa ; ultrastructure ; Helicobacter Infections ; pathology ; Helicobacter pylori ; Humans ; Intercellular Junctions ; ultrastructure ; Male ; Precancerous Conditions ; microbiology ; ultrastructure ; Stomach Neoplasms ; microbiology ; ultrastructure

OBJECTIVETo analyze the clinical characteristics and prognosis of the patients with gastric mucosa-associated lymphoid tissue (MALT) lymphoma.

METHODSThe clinical characteristics and prognostic factors of 103 gastric MALT lymphoma patients admitted to our hospital from April 2001 to August 2011 were retrospectively analyzed.

RESULTSThe onset of gastric MALT lymphoma was often insidious without specific clinical manifestation, the most common complaints were abdominal pain or discomfort, weight loss, poor appetite, nausea and vomiting. According to Musshoff staging system, 75(72.8%) patients were at early stages (I/II) and 28 (27.2%) patients at advanced stages (III/IV). There was no significant difference in five-year overall survival (OS) between the patients in surgery group and non-surgery group (60.4% vs 78.9%, respectively, P = 0072), while there was statistical difference in five-year progression-free survival (PFS) between the two groups (31.7% vs 52.8%, respectively, P = 0.023). Helicobacter pylori (Hp) was detected in 94 patients (91.2%). Anti-Hp treatment was effective with 100% overall response rate. In 94 patients with complete follow-up data, the 5-year OS rate was 75%, 5-year PFS rate was 46%. Univariate survival analysis showed that the B symptoms, Musshoff staging, performance staging, stage-modified IPI, levels of LDH, nodal involvement and levels of β(2)-microglobulin were correlated with OS and PFS (P < 0.05). The Cox regression analysis showed that Musshoff-III/IV stage, stage-modified IPI score > 2 and B symptoms were independent factor for OS (P < 0.05), whereas Musshoff-III/IV stage was independent factor for PFS (P = 0.027).

CONCLUSIONThe gastric MALT lymphoma had a favorable outcome with high OS rate. The anti-Hp therapy was an effective treatment for the gastric MALT lymphoma, which avoid the surgical trauma and improve the quality of life. The prognostic analysis showed that Musshoff staging, B symptoms or stage-modified IPI score were independent factors for OS and Musshoff staging was also an independent factor for PFS.

Adult ; Aged ; Aged, 80 and over ; Female ; Gastric Mucosa ; microbiology ; pathology ; Helicobacter Infections ; pathology ; Helicobacter pylori ; Humans ; Lymphoma, B-Cell, Marginal Zone ; diagnosis ; microbiology ; pathology ; Male ; Middle Aged ; Prognosis ; Retrospective Studies ; Stomach Neoplasms ; microbiology ; pathology ; Young Adult