Ogata R T, Levine R P
J Immunol. 1980 Oct;125(4):1494-8.
We have examined the effect of the antibiotic resistance plasmid, R100, on the complement (C) mediated killing of Escherichia coli K-12 strains. The viabilities, in dilute normal rabbit serum (NRS), of 5 such strains were compared with the viabilities of the same strains harboring R100. For 1 strain, J6-2, we also measured the effect of R100 on viability in normal human serum (NHS) and in guinea pig serum (GPS); in NRS, NHS,and GPS devoid of classical C pathway activity; and in NHS devoid of alternative pathway activity. Finally, we compared the depletion of individual complement components in sera exposed to J6-2 and J6-2 harboring R100. Our results demonstrate that 1) R100 renders E. coli K-12 resistant to killing by NRS, NHS, and GPS; 2) the level of resistance, which ranges from 30- to 10,000-fold, is strain dependent and serum dependent; 3) R100 inhibits killing by both the classical and alternative C pathway. Resistance appears to involve a disruption on the C pathway subsequent to the activation of C5.
我们研究了抗生素抗性质粒R100对补体(C)介导的大肠杆菌K-12菌株杀伤作用的影响。将5株此类菌株在稀释的正常兔血清(NRS)中的活力与携带R100的同一菌株的活力进行了比较。对于其中1株J6-2,我们还测定了R100对其在正常人血清(NHS)和豚鼠血清(GPS)中的活力的影响;在缺乏经典补体途径活性的NRS、NHS和GPS中;以及在缺乏替代途径活性的NHS中的影响。最后,我们比较了暴露于J6-2和携带R100的J6-2的血清中各个补体成分的消耗情况。我们的结果表明:1)R100使大肠杆菌K-12对NRS、NHS和GPS的杀伤产生抗性;2)抗性水平在30倍至10000倍之间,具有菌株依赖性和血清依赖性;3)R100抑制经典补体途径和替代补体途径的杀伤作用。抗性似乎涉及C5激活后补体途径的破坏。