Aydemir Selim A, Tekin Isak Ozel, Numanoglu Gamze, Borazan Ali, Ustundag Yucel
Department of Gastroenterology, Zonguldak Karaelmas University, Faculty of Medicine, Iç Hastaliklari ABD, Gastroenteroloji BD, 67800 Zonguldak, Turkey.
Mediators Inflamm. 2004 Dec;13(5-6):369-72. doi: 10.1155/S0962935104000559.
Helicobacter pylori is one of the main causes of gastroduodenal diseases, such as chronic gastritis and peptic ulcer. It has been shown that eosinophils increase in the stomach in H. pylori infection. Eosinophilic cationic protein (ECP) is a cytotoxic molecule secreted by the activated eosinophils. However, there are no sufficient data about the role of ECP in H. pylori infection and its effect on ulcer development. In this study we investigated the gastric eosinophilic infiltration, gastric juice and serum ECP levels in patients with chronic gastritis and gastric ulcer associated with H. pylori.
Forty-four H. pylori-positive and 20 H. pylori-negative patients who underwent upper gastrointestinal system endoscopy after admitting with dyspeptic complaints were enrolled in the study. Twenty-one of the H. pylori-positive patients had gastric ulcer while 23 patients had none. During endoscopy, multiple gastric biopsies and juices were taken. In gastric biopsies, H. pylori and eosinophilic infiltration were assessed. Additionally, gastric juice and serum ECP levels were measured.
Eosinophil infiltration, gastric juice ECP levels, and gastric juice/serum ECP ratios in the H. pylori-positive group were greater than in the H. pylori-negative group (p < 0.01). There was no statistically significant difference regarding serum ECP levels between the two groups (p > 0.05). When H. pylori-positive patients were compared with regard to gastric ulcer presence, however, there was no significant difference in gastric eosinophil infiltration, gastric juice ECP levels, serum ECP levels, and gastric juice/serum ECP ratios (p > 0.05).
The results of this study suggest that eosinophils and eosinophil-released ECP may contribute to inflammatory changes seen in chronic gastritis, whereas there is no proof that they play a role in ulcer development.
幽门螺杆菌是胃十二指肠疾病(如慢性胃炎和消化性溃疡)的主要病因之一。研究表明,幽门螺杆菌感染时胃内嗜酸性粒细胞会增多。嗜酸性阳离子蛋白(ECP)是活化嗜酸性粒细胞分泌的一种细胞毒性分子。然而,关于ECP在幽门螺杆菌感染中的作用及其对溃疡形成的影响,目前尚无充分的数据。在本研究中,我们调查了幽门螺杆菌相关慢性胃炎和胃溃疡患者的胃嗜酸性粒细胞浸润、胃液和血清ECP水平。
44例幽门螺杆菌阳性和20例幽门螺杆菌阴性患者因消化不良症状入院后接受上消化道系统内镜检查,纳入本研究。44例幽门螺杆菌阳性患者中,21例患有胃溃疡,另有23例未患胃溃疡。在内镜检查期间,采集了多个胃活检组织和胃液。在胃活检组织中,评估幽门螺杆菌和嗜酸性粒细胞浸润情况。此外,还测量了胃液和血清ECP水平。
幽门螺杆菌阳性组的嗜酸性粒细胞浸润、胃液ECP水平和胃液/血清ECP比值均高于幽门螺杆菌阴性组(p < 0.01)。两组之间血清ECP水平无统计学显著差异(p > 0.05)。然而,当比较幽门螺杆菌阳性患者有无胃溃疡时,胃嗜酸性粒细胞浸润、胃液ECP水平、血清ECP水平和胃液/血清ECP比值均无显著差异(p > 0.05)。
本研究结果表明,嗜酸性粒细胞和嗜酸性粒细胞释放的ECP可能导致慢性胃炎中出现的炎症变化,然而,尚无证据表明它们在溃疡形成中起作用。