Karch Helge, Friedrich Alexander W, Gerber Angela, Zimmerhackl Lothar B, Schmidt M Alexander, Bielaszewska Martina
Institut für Hygiene und Konsiliarlaboratorium für Hämolytisch-Urämisches Syndrom, Universitätsklinikum Münster, Münster, Germany.
Semin Thromb Hemost. 2006 Mar;32(2):105-12. doi: 10.1055/s-2006-939766.
Shiga toxin (Stx) subtyping suggests that the clinical outcome of infections caused by Shiga toxin-producing ESCHERICHIA COLI (STEC) depends, in large part, on the STX genotype of the infecting strain. Whereas the presence of the STX2 or STX2C genotype is associated with the ability of STEC to cause the hemolytic uremic syndrome (HUS), strains possessing STX2D or STX2E have been isolated from patients with less severe disease. In addition to the type of Stx, the level of Stx production might be critical for the pathogenicity of STEC. Control of Stx expression appears to be at the level of transcription. Injury to microvascular endothelial cells is the key event underlying the pathogenesis of HUS. We could show that in addition to Stx, STEC also produces other putative virulence factors, such as cytolethal distending toxin, which can contribute to the endothelial injury by interference with the cell cycle, which results in inhibition of cell proliferation and finally cell death.
志贺毒素（Stx）分型表明，产志贺毒素大肠杆菌（STEC）感染的临床结果在很大程度上取决于感染菌株的Stx基因型。虽然STX2或STX2C基因型的存在与STEC导致溶血尿毒综合征（HUS）的能力相关，但已从病情较轻的患者中分离出具有STX2D或STX2E的菌株。除了Stx类型外，Stx的产生水平可能对STEC的致病性至关重要。Stx表达的控制似乎在转录水平。微血管内皮细胞损伤是HUS发病机制的关键事件。我们可以证明，除了Stx外，STEC还产生其他假定的毒力因子，如细胞致死性膨胀毒素，它可通过干扰细胞周期导致内皮损伤，从而抑制细胞增殖并最终导致细胞死亡。
