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Epidermal growth factor and its receptor in chronic active gastritis and gastroduodenal ulcer before and after Helicobacter pylori eradication
Author(s) -
Chun Yu Wong B.,
Ping Wang W.,
Hau Leung So W.,
Shin V. Y.,
Man Wong W.,
Man Yee Fung F.,
Shiu Lam Liu E.,
Mo Hiu W.,
Kum Lam S.,
Hin Cho C.
Publication year - 2001
Publication title -
alimentary pharmacology and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.308
H-Index - 177
eISSN - 1365-2036
pISSN - 0269-2813
DOI - 10.1046/j.1365-2036.2001.01051.x
Subject(s) - helicobacter pylori , medicine , epidermal growth factor , gastritis , chronic gastritis , antrum , gastroenterology , gastric mucosa , spirillaceae , saliva , epidermal growth factor receptor , stomach , receptor
Background: Helicobacteria pylori infection of gastroduodenal mucosa is strongly associated with gastritis and peptic ulcer disease. The aims of the present study were to compare the gastroduodenal mucosal levels of epidermal growth factor (EGF) and its receptor (EGFR) among H. pylori ‐negative controls and H. pylori infected patients with chronic active gastritis or gastroduodenal ulcer before and after H. pylori eradication. Methods: The protein levels of EGF in mucosal tissues and saliva were determined by a solid‐phase enzyme‐linked immunosorbent assay (ELISA). Repeat transcription‐polymerase chain reaction and the following polymerase chain reaction ELISA were employed to examine the mucosal EGFR mRNA expression. Results: Mucosal injury and H. pylori infection increased EGF protein levels and EGFR mRNA expression in the antral mucosa. The concentration of EGF in saliva was not affected by mucosal damage or H. pylori infection. Successful H. pylori eradication normalized the EGFR mRNA back to its basal level 6 weeks after treatment. However, after unsuccessful eradication their high levels in the antrum persisted. All patients experienced ulcer healing after drug treatment, regardless of H. pylori eradication. Conclusions: Mucosal damage increased the expression of EGF protein and EGFR mRNA in the gastric mucosa. H. pylori could induce the expression of EGFR but not the EGF in the antral mucosa. The expression of EGFR could be a contributing factor for ulcer healing in patients with H. pylori infection.