Danielsson D, Jurstrand M
Department of Clinical Microbiology and Immunology, Orebro Medical Center Hospital, Sweden.
Dig Dis Sci. 1998 Sep;43(9 Suppl):167S-173S.
Some clinical isolates of nonopsonized H. pylori have the ability to activate neutrophils to an oxidative burst (neutrophil activating capacity, NAC), and such strains were significantly more often isolated from patients with peptic ulcer disease and active chronic gastritis. The purpose of the present work was to investigate the effect of rebamipide (Mucosta) on the release of reactive oxygen metabolites from neutrophils activated by various strains of H. pylori with or without NAC, nonopsonized or opsonized, using as controls fMLP and PMA, known activators of neutrophils, and to study the kinetics of these events by luminol-enhanced chemiluminescence and by flow cytometry. The results showed that the oxidative burst induced in neutrophils by fMLP and by nonopsonized or opsonized H. pylori with NAC was inhibited by rebamipide in a dose-dependent manner both in the early and late phases of activation. In contrast, the oxidative burst induced by opsonized H. pylori without NAC was not inhibited by rebamipide, which might indicate that it does not have the ability to block CR1 or CR3 receptors involved in opsonic phagocytosis but still has the ability to block the receptor(s) for NAC. The oxidative burst induced by PMA, which primarily activates protein kinase C, was not inhibited in the early phase but diminished 40-45% in the late phase with the 2 mM concentration of rebamipide, probably due to scavenging of reactive oxygen species. In conclusion, rebamipide has the ability to diminish the oxidative burst of neutrophils activated by nonopsonized or opsonized H. pylori organisms with neutrophil activating capacity, most likely through the blocking of fMLP-related receptors, inhibition of the production of reactive oxygen species, and the scavenging of such metabolites. Rebamipide may therefore be useful to prevent gastroduodenal lesions associated with gastric mucosal inflammation in H. pylori infection.
一些未调理的幽门螺杆菌临床分离株具有激活中性粒细胞产生氧化爆发的能力（中性粒细胞激活能力，NAC），并且这类菌株更常从消化性溃疡病和活动性慢性胃炎患者中分离出来。本研究的目的是研究瑞巴派特（胃仙-U）对不同幽门螺杆菌菌株（有无NAC、未调理或已调理）激活的中性粒细胞释放活性氧代谢产物的影响，以已知的中性粒细胞激活剂fMLP和PMA作为对照，并通过鲁米诺增强化学发光和流式细胞术研究这些事件的动力学。结果表明，fMLP以及未调理或已调理且具有NAC的幽门螺杆菌在中性粒细胞中诱导的氧化爆发在激活的早期和晚期均被瑞巴派特以剂量依赖的方式抑制。相比之下，无NAC的已调理幽门螺杆菌诱导的氧化爆发未被瑞巴派特抑制，这可能表明它没有阻断参与调理吞噬作用的CR1或CR3受体的能力，但仍有阻断NAC受体的能力。主要激活蛋白激酶C的PMA诱导的氧化爆发在早期未被抑制，但在晚期，2 mM浓度的瑞巴派特使其减少了40 - 45%，这可能是由于活性氧的清除。总之，瑞巴派特能够减少由具有中性粒细胞激活能力的未调理或已调理幽门螺杆菌激活的中性粒细胞的氧化爆发，最有可能是通过阻断与fMLP相关的受体、抑制活性氧的产生以及清除此类代谢产物。因此，瑞巴派特可能有助于预防幽门螺杆菌感染中与胃黏膜炎症相关的胃十二指肠病变。
