Galán J E, Pace J, Hayman M J
Department of Microbiology, School of Medicine, State University of New York, Stony Brook 11794.
Nature. 1992 Jun 18;357(6379):588-9. doi: 10.1038/357588a0.
Salmonella infection continues to be a major world-wide health problem. One essential pathogenic feature common to all Salmonella is their ability to penetrate the cells of the intestinal epithelium which are normally non-phagocytic. The internalization of Salmonella into mammalian cells is thought to be a receptor-mediated phenomenon and the invasion of cultured epithelial cells depends on several Salmonella genes, but nothing is known about the host determinants participating in this interaction. Protein tyrosine phosphorylation follows stimulation of many cell-surface receptors to initiate signal transduction pathways that stimulate cellular responses. We report here that invasion of cultured Henle-407 cells by Salmonella typhimurium induces the tyrosine phosphorylation of the epidermal growth factor (EGF) receptor. In contrast, an isogenic strain of S. typhimurium that is defective in invasion owing to a mutation in the invA gene is unable to induce such phosphorylation. Addition of EGF to cultured Henle-407 cells allowed the internalization of the invasion-defective S. typhimurium invA mutant although it did not cause the internalization of an adherent, but non-invasive, strain of Escherichia coli. This result indicates that stimulation of the EGF receptor is involved in the invasion of cultured Henle-407 cells by S. typhimurium.
沙门氏菌感染仍然是一个全球性的主要健康问题。所有沙门氏菌共有的一个重要致病特征是它们能够穿透通常不具有吞噬作用的肠道上皮细胞。沙门氏菌内化进入哺乳动物细胞被认为是一种受体介导的现象，培养的上皮细胞的侵袭取决于几个沙门氏菌基因，但对于参与这种相互作用的宿主决定因素却一无所知。蛋白质酪氨酸磷酸化在许多细胞表面受体受到刺激后发生，以启动刺激细胞反应的信号转导途径。我们在此报告，鼠伤寒沙门氏菌对培养的Henle-407细胞的侵袭会诱导表皮生长因子（EGF）受体的酪氨酸磷酸化。相比之下，由于invA基因突变而侵袭缺陷的鼠伤寒沙门氏菌同基因菌株无法诱导这种磷酸化。向培养的Henle-407细胞中添加EGF可使侵袭缺陷的鼠伤寒沙门氏菌invA突变体内化，尽管它不会导致黏附但不具有侵袭性的大肠杆菌菌株内化。这一结果表明，EGF受体的刺激参与了鼠伤寒沙门氏菌对培养的Henle-407细胞的侵袭。
