Impact of bacterial eradication on the cell proliferation and p53 protein accumulation in Helicobacter pylori-associated gastritis.
BACKGROUND
This study investigates the cell proliferation and the expression of p53 protein in Helicobacter pylori (H. pylori)-associated gastritis and assesses the effect of bacterial eradication on these epithelial factors.


METHODS
Seventy-nine patients with H. pylori-associated gastritis were randomized into the control group (n = 38) and anti-H. pylori group (n = 41). Each patient received endoscopic examinations with gastric biopsy before and 8 weeks after the treatment. The specimens from gastric antrum were immunostained for monoclonal antibodies against the proliferating cell nuclear antigen (PCNA) and p53 protein.


RESULTS
In the control group, the total labeling index (L.I.) of PCNA and the positive index (P.I.) of p53 in the whole foveolar epithelium were unchanged after treatment. In the anti-H. pylori group, 35 of 41 cases (85.3%) achieved eradication of H. pylori. Amongst the H. pylori-eradicated cases, the total L.I. of PCNA in the whole foveolar epithelium did not meaningfully alter after H. pylori elimination (p > 0.05). However, a significant reduction of L.I. was observed in the middle compartments of the gastric pits (before vs. after treatment: 14.0 vs. 7.3, p < 0.05). With regard to the p53 expression, the P.I.s were significantly decreased in the whole foveolar epithelium (before vs. after treatment: 0.57 vs. 0.17, p < 0.05) and in each compartment of the gastric pits (before vs. after treatment: [upper compartment]: 0.34 vs. 0.15, p < 0.05; [middle compartment]: 0.67 vs. 0.23, p < 0.05; [lower compartment]: 0.71 vs. 0.20, p < 0.05) after eradication of H. pylori.


CONCLUSIONS
Bacterial eradication reverses the hyperproliferating status of the foveolar epithelium in patients with H. pylori gastritis and leads to a decrease in p53 accumulation in the epithelial cells.
Hsu
P I
PI
Department of Internal Medicine, Veterans General Hospital-Kaohsiung, Taiwan, ROC.
Lai
K H
KH
Chien
E J
EJ
Lin
C K
CK
Lo
G H
GH
Jou
H S
HS
Cheng
J S
JS
Chan
H H
HH
Hsu
J H
JH
Ger
L P
LP
Hsu
P N
PN
Tseng
H H
HH
D053799:2-Pyridinylmethylsulfinylbenzimidazoles; D000863:Antacids / Q000627:therapeutic use; D000900:Anti-Bacterial Agents / Q000627:therapeutic use; D001284:Atrophy; D002455:Cell Division; D004359:Drug Therapy, Combination / Q000627:therapeutic use*; D005260:Female; D005756:Gastritis / Q000188:drug therapy* / Q000382:microbiology / Q000473:pathology*; D016481:Helicobacter Infections / Q000188:drug therapy* / Q000473:pathology*; D016480:Helicobacter pylori; D006801:Humans; D007150:Immunohistochemistry; D064747:Lansoprazole; D008297:Male; D008679:Metaplasia; D008795:Metronidazole / Q000627:therapeutic use*; D008875:Middle Aged; D009853:Omeprazole / Q000031:analogs & derivatives* / Q000627:therapeutic use; D009942:Organometallic Compounds / Q000627:therapeutic use; D018809:Proliferating Cell Nuclear Antigen / Q000032:analysis; D013752:Tetracycline / Q000627:therapeutic use*; D016159:Tumor Suppressor Protein p53 / Q000032:analysis*
D053799:2-Pyridinylmethylsulfinylbenzimidazoles; D000863:Antacids; D000900:Anti-Bacterial Agents; D009942:Organometallic Compounds; D018809:Proliferating Cell Nuclear Antigen; D016159:Tumor Suppressor Protein p53; D064747:Lansoprazole; D008795:Metronidazole; D013752:Tetracycline; C002791:bismuth tripotassium dicitrate; D009853:Omeprazole