Falzano L, Rivabene R, Santini M T, Fabbri A, Fiorentini C
Department of Ultrastructures, Istituto Superiore di Sanità, Viale Regina Elena 299, Rome, 00161, Italy.
Biochem Biophys Res Commun. 2001 May 25;283(5):1026-30. doi: 10.1006/bbrc.2001.4894.
Cytotoxic Necrotizing Factor 1 (CNF1) is a protein toxin from Escherichia coli that induces the activation of Rho, Rac, and Cdc42 GTPases, all involved in actin reorganization. Rac plays a further role in oxidase function. In epithelial cells, CNF1 has been reported to induce a phagocytic-like behavior in terms of a ruffle-driven ingestion of large material. We herein show that CNF1-activated epithelial cells may exert additional cell responses typical of professional phagocytes following stimulation, i.e., an increase in oxygen consumption and the generation of superoxide anions. Such effects were triggered by the contact of latex beads with epithelial cells and were significantly augmented by CNF1-induced Rac activation. Altogether our data indicate that Rac, one of the targets of CNF1, plays a pivotal role in these phenomena, suggesting the involvement in epithelial cells of a Rac-dependent NADPH-oxidase complex similar to that employed by professional phagocytes.
细胞毒性坏死因子1(CNF1)是一种来自大肠杆菌的蛋白质毒素,它能诱导Rho、Rac和Cdc42 GTP酶的激活,这些酶都参与肌动蛋白重组。Rac在氧化酶功能中发挥进一步作用。据报道,在上皮细胞中,CNF1会诱导一种类似吞噬的行为,即通过褶皱驱动摄取大的物质。我们在此表明,CNF1激活的上皮细胞在受到刺激后可能会表现出专业吞噬细胞特有的其他细胞反应,即耗氧量增加和超氧阴离子的产生。这些效应是由乳胶珠与上皮细胞的接触引发的,并因CNF1诱导的Rac激活而显著增强。我们的数据总体表明,CNF1的靶标之一Rac在这些现象中起关键作用,这表明上皮细胞中存在一种类似于专业吞噬细胞所使用的依赖Rac的NADPH氧化酶复合物。