Nakane Akio, Sasaki Sanae
Department of Bacteriology, Hirosaki University School of Medicine.
Nihon Rinsho. 2002 Jun;60(6):1089-94.
Shiga toxins(Stxs), which are produced by enterohemorrhagic Escherichia coli and Shigella dysenteriae serotype I, induce proinflammatory cytokines including tumor necrosis factor-alpha, interleukin(IL)-1 beta, IL-6, interferon-gamma, and chemokines such as IL-8 in intestinal epithelial cells, vascular endothelial cells, and monocytes/macrophages in vitro and in kidneys and spleen in vivo. Cytokines induced by Stxs and lipopolysaccharide enhance the toxicity of Stxs via up-regulation of the expression of Gb3, a Stx receptor, and infiltration of neutrophils. Stxs bind to neutrophils and transmigrate across intestinal mucosa and are transported to the target organs through bloodstreams. Stxs induce cytokines in vascular endothelial cells and peripheral blood monocytes and may injure organ tissues, finally resulting in hemolytic uremic syndrome and encephalopathia.
志贺毒素(Stxs)由肠出血性大肠杆菌和痢疾志贺菌血清型1产生,在体外可诱导肠上皮细胞、血管内皮细胞和单核细胞/巨噬细胞产生促炎细胞因子,包括肿瘤坏死因子-α、白细胞介素(IL)-1β、IL-6、干扰素-γ,以及趋化因子如IL-8,在体内可在肾脏和脾脏中诱导产生。由志贺毒素和脂多糖诱导产生的细胞因子通过上调志贺毒素受体Gb3的表达以及中性粒细胞的浸润来增强志贺毒素的毒性。志贺毒素与中性粒细胞结合并穿过肠黏膜迁移,通过血流运输到靶器官。志贺毒素在血管内皮细胞和外周血单核细胞中诱导产生细胞因子,并可能损伤器官组织,最终导致溶血尿毒综合征和脑病。