Increased production of interleukin 1 I and hepatocyte growth factor may contribute to foveolar hyperplasia in enlarged fold gastritis

Accepted for publication 20 June 1996 Abstract Background and Aims-It has been reported that eradication of Helicobacter pylon improves fold width in H pylon associated enlarged fold gastritis. The aim of this study was to clarify the mechanism offold thickening in this condition. Patients and Methods-In eight patients with enlarged fold gastritis and 13 patients without enlarged folds, the presence of H pylori infection, inflammatory infiltrates, mucosal plasia, and epithelial cell proliferation in the body mucosa were investigated, and production of transforming growth factor a (TGFa), hepatocyte growth factor (HGF), and interleukin 1p (IL 1,) was determined by a competitive reverse transcription/polymerase chain reaction method and in vitro short-term culture ofbiopsy specimens. Results-In the patients with enlarged fold gastritis, inflammatory infiltrates including macrophages increased with H pylon colonisation in the body. Foveolar thickness and proliferating celi nuclear antigen (PCNA) labelling index were increased. Messenger RNA levels of HGF, but not TGFa, were increased, and release ofHGF and IL 1 was increased. HGF release, which was positively correlated with IL 1 release and foveolar thickness, decreased in the presence ofIL 1 receptor antagonist. After eradication of H pylon, inflammatory infiltrates, IL 10 and HGF release decreased with concomitant decreases in PCNA labelling index, foveolar thickness and fold width. Conclusions-Increased IL 1 and HGF production caused by H pylon infection may contribute to fold thickening of the stomach by stimulating epithelial cell proliferation and foveolar hyperplasia in patients with enlarged fold gastritis. (Gut 1996; 39: 787-794)