Yoshikawa T, Naito Y
First Department of Medicine, Kyoto Prefectural University of Medicine, Japan.
Free Radic Res. 2000 Dec;33(6):785-94. doi: 10.1080/10715760000301301.
Gastric inflammation is a highly complex biochemical protective response to cellular/tissue injury. When this process occurs in an uncontrolled manner, the result is excessive cellular/tissue damage that results chronic inflammation and destruction of normal tissue. Current evidence suggests that Helicobacter pylori (H. pylori) infection and nonsteroidal anti-inflammatory drug (NSAID) ingestion are major causative factors in the pathogenesis of gastric mucosal injury in humans. In response to H. pylori infection or NSAID, neutrophils are recruited to the site of inflammation and generate reactive oxygen and nitrogen species and proteases. However, neutrophils are not able to kill the bacteria that live in the gastric mucus, and compounds produced by activated neutrophils themselves may be potentially harmful for normal tissue. It has been shown that leukocyte-vascular endothelial cell interaction is regulated by various cell adhesion molecules, and that this interaction is directly or indirectly modified by many factors, the origin of which is H. pylori and NSAIDs. This review describes the potential role of neutrophils and neutrophil-associated inflammation for gastric oxidative stress and injury induced by H. pylori and/or NSAID.
胃炎症是对细胞/组织损伤的一种高度复杂的生化保护反应。当这个过程以不受控制的方式发生时，结果是细胞/组织过度损伤，导致慢性炎症和正常组织的破坏。目前的证据表明，幽门螺杆菌（H. pylori）感染和非甾体抗炎药（NSAID）的摄入是人类胃黏膜损伤发病机制中的主要致病因素。针对幽门螺杆菌感染或非甾体抗炎药，中性粒细胞被募集到炎症部位，并产生活性氧和氮物质以及蛋白酶。然而，中性粒细胞无法杀死生活在胃黏液中的细菌，并且活化的中性粒细胞自身产生的化合物可能对正常组织有潜在危害。已经表明，白细胞与血管内皮细胞的相互作用受多种细胞粘附分子调节，并且这种相互作用直接或间接受许多因素影响，这些因素源于幽门螺杆菌和非甾体抗炎药。这篇综述描述了中性粒细胞以及与中性粒细胞相关的炎症在幽门螺杆菌和/或非甾体抗炎药诱导的胃氧化应激和损伤中的潜在作用。
