Effect of Helicobacter pylori infection and eradication on gastric epithelial cell proliferation and apoptosis.
OBJECTIVE
the effect of Helicobacter pylori infection on gastric epithelial cell proliferation and apoptosis is still controversial. Our aim was to evaluate the effect of H. pylori infection on cell kinetic parameters in normal gastric epithelium, gastritis with/without intestinal metaplasia and gastric cancer.


METHODS
antral biopsies were taken from 121 patients (61 women, 60 men, mean age 58.5+/-14.3 years of age) who underwent routine gastroscopy for upper gastrointestinal symptoms. Sections were scored for normal epithelia (n=15), gastritis without intestinal metaplasia (n=74), gastritis with intestinal metaplasia (n=24), and gastric adenocarcinoma (n=8). Fifty-two patients had H. pylori positive gastritis, and success of H. pylori eradication therapy was controlled in 12 cases, all with intestinal metaplasia. To characterize cell proliferation and assess apoptosis, immunohistochemistry [Proliferating Cell Nuclear Antigen (PCNA)], histochemistry [Argyrophil Nucleolar Organizer Regions (AgNOR)], and terminal deoxynucleotidyl transferase (TdT)-mediated deoxyuridinetriphosphate (dUTP) nick end-labeling (TUNEL) were used, respectively.


RESULTS
both cell proliferation and apoptosis is was higher in chronic gastritis when compared with normal epithelia, but neither PCNA LI (54.79+/-19.1 vs. 53.20+/-20.7) nor AgNOR counts (291.43+/-44.3 vs. 277.8+/-57.54) were different in H. pylori positive versus negative chronic gastritis. A significant positive correlation (P<0.05) was found in this group between PCNA and AgNOR techniques. Apoptosis was significantly higher (P<0.05) in H. pylori positive cases only when intestinal metaplasia was not present. Cell proliferation in intestinal metaplasia decreased to the activity of normal epithelium after successful eradication of H. pylori but remained high if eradication therapy failed.


CONCLUSIONS
epithelial cell proliferation does not depend on H. pylori status in chronic gastritis. H. pylori increases apoptosis only in the absence of intestinal metaplasia.
Unger
Z
Z
Second Department of Internal Medicine, Clinical Gastroenterology and Endocrinology Unit, Semmelweis University, Budapest, Hungary.
Molnár
B
B
Szaleczky
E
E
Törgyekes
E
E
Müller
F
F
Zágoni
T
T
Tulassay
Z
Z
Prónai
L
L
D000230:Adenocarcinoma / Q000473:pathology; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000900:Anti-Bacterial Agents / Q000627:therapeutic use; D017209:Apoptosis; D002453:Cell Cycle; D002455:Cell Division; D005260:Female; D005753:Gastric Mucosa / Q000473:pathology* / Q000503:physiopathology*; D016481:Helicobacter Infections / Q000188:drug therapy / Q000473:pathology*; D016480:Helicobacter pylori; D006801:Humans; D007422:Intestines / Q000473:pathology; D008297:Male; D008679:Metaplasia; D008875:Middle Aged; D013274:Stomach Neoplasms / Q000473:pathology
D000900:Anti-Bacterial Agents