Vuopio-Varkila J
National Public Health Institute, Helsinki, Finland.
J Med Microbiol. 1988 Jan;25(1):33-9. doi: 10.1099/00222615-25-1-33.
An experimental Escherichia coli septicaemia-peritonitis model was adapted to immunosuppressed mice. The mice were made neutropenic by a sublethal dose of cyclophosphamide, which resulted in a 100-fold increase in their susceptibility to intraperitoneal injection of E. coli O18:K1. A lethal infection could be prevented by passive immunisation with anti-K1 capsular or anti-O18 LPS antibodies but not with anti-J5 bacterial antibodies. The anti-K1 and anti-O18 antisera were able to increase the LD50 of the E. coli challenge by factors of 50 and 5, respectively. The role of non-specific, lipopolysaccharide (LPS)-mediated resistance to infection was also investigated in this model, in which only long-living phagocytic cells such as macrophages are believed to be functional. Pretreatment of mice with LPS was shown to prevent growth of the bacterial challenge in the peritoneal cavity and blood and to result in a five-fold increase in the LD50 of the challenge strain. These findings suggest an important role for macrophages as effector cells in defence against E. coli infection.
一种实验性大肠杆菌败血症 - 腹膜炎模型被应用于免疫抑制小鼠。通过亚致死剂量的环磷酰胺使小鼠中性粒细胞减少,这导致它们对腹腔注射大肠杆菌O18:K1的易感性增加了100倍。用抗K1荚膜或抗O18脂多糖抗体进行被动免疫可预防致死性感染,但用抗J5细菌抗体则不能。抗K1和抗O18抗血清能够分别将大肠杆菌攻击的半数致死剂量(LD50)提高50倍和5倍。在该模型中还研究了非特异性的、脂多糖(LPS)介导的抗感染作用,在这个模型中,据信只有诸如巨噬细胞等长寿吞噬细胞具有功能。结果表明,用LPS预处理小鼠可防止攻击细菌在腹腔和血液中生长,并使攻击菌株的LD50增加五倍。这些发现表明巨噬细胞作为效应细胞在抵抗大肠杆菌感染中发挥着重要作用。