A Review: Relation between Invasiveness and the K1 Capsular Polysaccharide of Escherichia coli
A Review: Relation between Invasiveness and the K1 Capsular Polysaccharide of Escherichia coli
复制标题
大肠杆菌侵袭力与K1荚膜多糖的关系综述
作者：
M. Schiffer;Elizabeth Oliveira;M. Glodé;G. Mccracken;Larry M Sarff;J. Robbins
我们迄今为止的研究结论可总结如下。 (1)将引起新生儿脑膜炎的侵袭性大肠杆菌菌株封装起来。诱发脑膜炎的菌株中至少 80% 是 K1，从患有败血症但没有脑膜炎的婴儿中分离出的菌株中大约 40% 也是 K1。侵袭性与 K1 抗原最相关，而不是与大肠杆菌 O 和 H 抗原相关。 (2)脑脊液菌株荚膜含量与其侵袭性无关。与局限于膀胱或粪便中的大肠杆菌相比，侵入肾实质的大肠杆菌的 K 荚膜多糖含量和分子量更高，与此相反，DSF K1 菌株之间没有差异。关于酸性荚膜多糖赋予的侵入特性的机制的推测可以源自文献。未封装的或“粗糙的细菌”对无丙种球蛋白血症血清的杀菌作用敏感(15, 53)。当注射到初初乳前（无丙种球蛋白血症但含有补体）、剖腹产和抗原剥夺的仔猪中时，未包膜的细菌会迅速从循环中清除。相比之下，注射到这些相同动物体内的光滑细菌在没有可检测到的脾脏或肝脏清除的情况下进行循环、繁殖，并导致这些动物的死亡。包膜细菌的耐药机制被认为是由于难以接近能够激活替代补体途径系统的深层体细胞抗原结构。因此，调理作用和其他宿主补体依赖性活性可能必然是包膜细菌的抗体介导的。封装生物体的这种补体抗性可能是定量的，应该进行研究以确定各种 K1 大肠杆菌菌株之间的差异。 (3)K1株在婴儿、儿童和成人中广泛流行，并能迅速传播给婴儿。在大多数情况下，患病婴儿的感染菌株的来源是母亲。然而，我们的研究证明，来自服务员的传播也是一种可能的机制。 (4)血清抗荚膜抗体在动物模型中的保护作用已得到证实。我们的初步观察结果表明，普通人群血清 K1 抗体水平较低，而且迄今为止研究的两种动物物种中 K1 抗体主要为 IgM，这表明初乳 K1 抗体可能在赋予对该疾病的免疫力方面发挥重要作用。
The conclusions from our studies to date may be summarized as follows. (1) Invasive E. coli strains causing neonatal meningitis are encapsulated. At least 80% of those strains inducing mengitis are K1 and approximately 40% of those strains isolated from infants with septicemia but without meningitis are also K1. Invasiveness is best related to the K1 antigen and not to E. coli O and H antigens. (2) The capsular content of CSF strains is not related to their invasiveness. In contrast to observations reporting higher K capsular polysaccharide content and molecular weight of E. coli invading the renal parenychma as compared with those E. coli confined to the bladder or in the stool, there were no differences among DSF K1 strains. Sepculation as to the mechanism of the invasive properties conferred by acidic capsular polysaccharides may be derived from the literature. Unencapsulated or "rough bacteria" are susceptible to the bactericidal action of agammaglobulinemice sera (15, 53). When injected into precolostral (agammaglobulinemic but complement containing), cesarian-delivered, and antigen-deprived piglets, unencapsulated bacteria are rapidly cleared from the circulation. In contrast, smooth bacteria injected into these same animals circulate without detectable splenic or hepatic clearance, multiply, and result in the death of these animals. The mechanism of the resistance of encapsulated bacteria has been postulated to be due to the inaccessibility of the deep somatic antigen structures capable of activating the alternate complement pathway system. Thus, opsoninization and other host complement-dependent activities may of necessity be antibody mediated for encapsulated bacteria. This complement resistance of encapsulated organisms may be quanititative and studies should be done to determine differences among various K1 E. coli strains. (3) K1 strains are widely prevalent among infants, children, and adults and are quickly transmitted to infants. In most cases the source of the infecting strain in diseased infants is the mother. However, transmission from attendants, demonstrable in our studies, is also a possible mechanism. (4) A protective role of serum anticapsular antibodies in animal models has been demonstrated. Our initial observations indicating low serum K1 antibodies in the general population and the finding that K1 antibodies are predominantly IgM in two animal species studied so far suggest that colostral K1 antibodies may be important in conferring immunity to this disease.