杀白细胞素ED(leukocidin ED，LukED)是金黄色葡萄球菌产生的双组分成孔杀白细胞素之一，由共转录于一条mRNA的lukE和lukD两个基因编码。LukED可与趋化因子受体CCR5结合以杀伤巨噬细胞、T细胞和树突细胞，或与中性粒细胞、单核细胞和自然杀伤(natural kiler，NK)细胞上的表面受体CXCR1/2结合以促进金黄色葡萄球菌的致病性及系统性感染宿主的死亡。此外，LukED还可结合Duffy 抗原趋化因子受体，使裂解红细胞释放血红蛋白，促进细菌的铁吸收和生长繁殖。LukED的表达受双组分信号转导系统附属基因调节子——毒素抑制子(Agr-Rot)通路和转录调节子RpiRc、SpoVG的调控。lukED基因在金黄色葡萄球菌中广泛流行，与金黄色葡萄球菌所致血流感染、脓疱病及抗生素相关性腹泻密切相关。这些进展对了解LukED的表达调控机制、临床意义及其在细菌致病机制中的作用，开发新的金黄色葡萄球菌感染抗毒素治疗药物具有重要意义

As a member of bicomponent pore-forming leucocidins from Staphylococcus aureus (S. aureus), leukocidin ED (LukED) is encoded by two linked genes (lukE and lukD), which are co-transcribed into one mRNA. LukED is found to be able to target the chemokine receptor CCR5 to kill inflammatory macrophages, T cells, and dendritic cells, or to target receptor CXCR1/2 on neutrophils, monocytes and natural killer (NK) cells to enhance pathogenicity of S. aureus and death of the host. In addition, LukED can also lyse erythrocytes to release hemoglobin by binding to the Duffy antigen receptor for chemokines, and further promote the absorption of iron and growth of bacteria. The expression of LukED is regulated by the accessory gene regulatory-repressor of toxins (agr-rot) pathway and transcriptional regulators such as RpiRc and SpoVG. Studies show that lukED genes have a high frequency in S. aureus and have a close association with bloodstream infection, impetigo and antibiotic-associated diarrhea. Progress on researches of LukED not only improves our knowledge about clinical importance and the pathogenesis of S. aureus, but also provides insight into the development of potential novel anti-toxin drugs for the treatment of S. aureus infection.