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

No abstract available.
Bacteria/*isolation & purification ; Female ; Gastric Mucosa/*microbiology ; Gastritis/*microbiology ; Humans ; Intestinal Diseases/*microbiology ; Male ; *Microbiota

Adolescent ; Child ; Child, Preschool ; Female ; Gastric Mucosa ; microbiology ; Gastrointestinal Diseases ; diagnosis ; microbiology ; Helicobacter Infections ; diagnosis ; microbiology ; Helicobacter pylori ; growth & development ; isolation & purification ; Humans ; Infant ; Male ; Mouth Mucosa ; microbiology

BACKGROUND: About half of the world population is infected with H. pylori, but the transmission and the source of this infection are still unclear. Recently, dental plaque (DP) and saliva have been implicated as possible sources of H. pylori infection. This study was done to investigate the detection rates of H. pylori in the DP and saliva by use of PCR depending on H. pylori infection state of gastric mucosa. METHODS: In 46 subjects, gastric H. pylori colonization was evaluated with CLO test, microscopy of Gram stained mucosal smear, culture and histology after modified Giemsa staining in the antrum and body, respectively. A patient was regarded as H. pylori positive if one or more of the four aforementioned test methods demonstrated H. pylori colonization of the gastric mucosa. For detection of H. pylori in the DP and saliva, PCR assay was done with ET4-U and ET4-L primers. To estimate the sensitivity and specificity of this PCR, H. pylori positivity was evaluated in the antrum and body, separately. RESULTS: The sensitivity of mucosal PCR was 50.0% (27/54) and the specificity 86.8% (33/38). When a subject was regarded as H. pyloi positive, if either antrum or body mucosal H. pylori was is positive, the positive rate of mucosal PCR was 62.1% (18 subjects) in the 29 H. pylori-positive and 17.6% (3 subjects) in the 17 H. pylori-negative subjects. DP PCR was positive in 2 of 29 H. pylori-positive subjects (6.9%) and none in the 17 H. pylori-negative (0%). Saliva PCR was positive in 4 of 14 H. pylori-positive subjects (28.6%) and none of 6 H. pylori-negative (0%). CONCLUSION: The detection rates of H. pylori in DP and saliva by PCR were rather low, 6.9% and 28.6%, respectively, and these rates might have been underestimated by low sensitivity of the PCR method used in this study. However, the results that H. pylori was found in the DP and saliva suggest that the oral cavity can perform a role as a reservoir of H. pylori in Korea.
Dental Plaque/microbiology* ; Gastric Mucosa/microbiology ; Helicobacter pylori/isolation & purification* ; Human ; Polymerase Chain Reaction ; Saliva/microbiology* ; Sensitivity and Specificity

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

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

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

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

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

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