Yasunaga Y, Shinomura Y, Kanayama S, Higashimoto Y, Yabu M, Miyazaki Y, Kondo S, Murayama Y, Nishibayashi H, Kitamura S, Matsuzawa Y
Second Department of Internal Medicine, Osaka University Medical School, Japan.
Gut. 1996 Dec;39(6):787-94. doi: 10.1136/gut.39.6.787.
It has been reported that eradication of Helicobacter pylori improves fold width in H pylori associated enlarged fold gastritis. The aim of this study was to clarify the mechanism of fold thickening in this condition.
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 alpha (TGF alpha), hepatocyte growth factor (HGF), and interleukin 1 beta (IL 1 beta) was determined by a competitive reverse transcription/polymerase chain reaction method and in vitro short-term culture of biopsy specimens.
In the patients with enlarged fold gastritis, inflammatory infiltrates including macrophages increased with H pylori colonisation in the body. Foveolar thickness and proliferating cell nuclear antigen (PCNA) labelling index were increased. Messenger RNA levels of HGF, but not TGF alpha, were increased, and release of HGF and IL 1 beta was increased. HGF release, which was positively correlated with IL 1 beta release and foveolar thickness, decreased in the presence of IL 1 receptor antagonist. After eradication of H pylori, inflammatory infiltrates, IL 1 beta and HGF release decreased with concomitant decreases in PCNA labelling index, foveolar thickness and fold width.
Increased IL 1 beta and HGF production caused by H pylori infection may contribute to fold thickening of the stomach by stimulating epithelial cell proliferation and foveolar hyperplasia in patients with enlarged fold gastritis.
据报道，根除幽门螺杆菌可改善幽门螺杆菌相关性胃黏膜皱襞增粗。本研究旨在阐明这种情况下皱襞增厚的机制。
对8例胃黏膜皱襞增粗的患者和13例无皱襞增粗的患者，研究胃体黏膜中幽门螺杆菌感染、炎症浸润、黏膜化生及上皮细胞增殖情况，并采用竞争性逆转录/聚合酶链反应法及活检标本体外短期培养法测定转化生长因子α（TGFα）、肝细胞生长因子（HGF）及白细胞介素1β（IL-1β）的产生。
胃黏膜皱襞增粗的患者中，胃体部巨噬细胞等炎症浸润随幽门螺杆菌定植而增加。胃小凹厚度及增殖细胞核抗原（PCNA）标记指数升高。HGF的信使核糖核酸水平升高，而TGFα未升高，且HGF和IL-1β的释放增加。HGF释放与IL-1β释放及胃小凹厚度呈正相关，在存在IL-1受体拮抗剂时降低。根除幽门螺杆菌后，炎症浸润、IL-1β及HGF释放减少，同时PCNA标记指数、胃小凹厚度及皱襞宽度也随之降低。
幽门螺杆菌感染导致的IL-1β和HGF产生增加，可能通过刺激胃黏膜皱襞增粗患者的上皮细胞增殖和胃小凹增生，从而促使胃皱襞增厚。
