Cardiff University, School of Medicine, Department of Child Health, University Hospital of Wales, Heath Park, Cardiff, UK.
Immunobiology. 2012 Feb;217(2):187-94. doi: 10.1016/j.imbio.2011.07.009. Epub 2011 Jul 12.
Many Gram-negative bacteria, unlike Gram-positive, are directly lysed by complement. Ureaplasma can cause septic arthritis and meningitis in immunocompromised individuals and induce premature birth. Ureaplasma has no cell wall, cannot be Gram-stain classified and its serum susceptibility is unknown.
Survival of Ureaplasma serovars (SV) 1, 3, 6 and 14 (collectively Ureaplasma parvum) were measured following incubation with normal or immunoglobulin-deficient patient serum (relative to heat-inactivated controls). Blocking monoclonal anti-C1q antibody and depletion of calcium, immunoglobulins, or lectins were used to determine the complement pathway responsible for killing.
Eighty-three percent of normal sera killed SV1, 67% killed SV6 and 25% killed SV14; greater killing correlating to strong immunoblot identification of anti-Ureaplasma antibodies; killing was abrogated following ProteinA removal of IgG1. All normal sera killed SV3 in a C1q-dependent fashion, irrespective of immunoblot identification of anti-Ureaplasma antibodies; SV3 killing was unaffected by total IgG removal by ProteinG, where complement activity was retained. Only one of four common variable immunodeficient (CVID) patient sera failed to kill SV3, despite profound IgM and IgG deficiency for all; however, killing of SV3 and SV1 was restored with therapeutic intravenous immunoglobulin therapy.
Only the classical complement pathway mediated Ureaplasma-cidal activity, sometimes in the absence of observable immunoblot reactive bands.
与革兰氏阳性菌不同，许多革兰氏阴性菌可被补体直接溶解。解脲支原体可引起免疫功能低下个体的败血症性关节炎和脑膜炎，并可导致早产。解脲支原体无细胞壁，不能进行革兰氏染色分类，其血清敏感性未知。
用正常或免疫球蛋白缺乏患者血清（相对于热失活对照）孵育后，测量解脲支原体血清型 1、3、6 和 14（统称为解脲支原体微小脲原体）的存活情况。使用阻断单克隆抗 C1q 抗体和耗尽钙、免疫球蛋白或凝集素来确定负责杀伤的补体途径。
83%的正常血清可杀死 SV1，67%的血清可杀死 SV6，25%的血清可杀死 SV14；杀伤作用与抗解脲支原体抗体的强烈免疫印迹鉴定相关；用 ProteinA 去除 IgG1 后，杀伤作用被阻断。所有正常血清均以 C1q 依赖的方式杀死 SV3，而与抗解脲支原体抗体的免疫印迹鉴定无关；用 ProteinG 去除总 IgG 不影响补体活性，SV3 的杀伤作用不受影响。尽管所有患者的 IgM 和 IgG 均严重缺乏，但四名常见可变免疫缺陷（CVID）患者的血清中只有一种未能杀死 SV3；然而，SV3 和 SV1 的杀伤作用在接受静脉注射免疫球蛋白治疗后得到恢复。
只有经典补体途径介导解脲支原体杀伤活性，有时在缺乏可观察到的免疫印迹反应带的情况下也是如此。
