Singh A, LeChevallier M W, McFeters G A
Appl Environ Microbiol. 1985 Aug;50(2):406-11. doi: 10.1128/aem.50.2.406-411.1985.
A sublethal concentration of copper (0.75 mg/liter) caused substantial injury (87 to 95%) of Yersinia enterocolitica serotype O:8 cells in 72 h at 4 degrees C without producing extensive cell death. Copper-injured cells had a higher 50% lethal dose in mice (2,700 CFU) than uninjured cells (150 CFU). This reduced virulence correlated with more rapid clearance of the injured cells from the blood of mice after intravenous inoculation. A possible role of the liver in this process was shown by significant cell accumulation in mouse livers when copper-injured Y. enterocolitica cells were administered, compared with uninjured bacteria. In vitro studies with isolated mouse liver membranes showed higher titers of aggregation with copper-injured cells than control cells. The in vitro aggregation reaction and blood clearance activity in vivo were abolished by sugars that are known to interact with a hepatic lectin. Our data suggest that copper-induced injury reduces the virulence of Y. enterocolitica and that the liver may be involved in nonimmune rapid clearance of the injured cells, probably by interaction with a hepatic lectin(s).
亚致死浓度的铜(0.75毫克/升)在4℃下72小时内对小肠结肠炎耶尔森菌O:8血清型细胞造成了严重损伤(87%至95%),但未导致大量细胞死亡。铜损伤的细胞在小鼠体内的50%致死剂量(2700 CFU)高于未损伤的细胞(150 CFU)。这种毒力降低与静脉接种后损伤细胞从小鼠血液中更快清除有关。当接种铜损伤的小肠结肠炎耶尔森菌细胞时,与未损伤的细菌相比,小鼠肝脏中出现明显的细胞积聚,这表明肝脏在这一过程中可能发挥作用。对分离的小鼠肝细胞膜进行的体外研究表明,与对照细胞相比,铜损伤细胞的凝集滴度更高。已知与肝凝集素相互作用的糖类可消除体外凝集反应和体内血液清除活性。我们的数据表明,铜诱导的损伤降低了小肠结肠炎耶尔森菌的毒力,肝脏可能参与了对损伤细胞的非免疫性快速清除,可能是通过与一种或多种肝凝集素相互作用实现的。