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首页> 外文期刊>Infection and immunity >Deposition of complement components on Streptococcus agalactiae in bovine milk in the absence of inflammation.
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Deposition of complement components on Streptococcus agalactiae in bovine milk in the absence of inflammation.

机译：在无炎症的情况下，牛乳中无乳链球菌上补体成分的沉积。

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Bovine milk is generally considered to be almost devoid of complement, on the basis of undetectable hemolytic activity, unless inflammation recruits plasma components. This study examines the deposition of complement components on a mastitis-causing isolate of Streptococcus agalactiae by enzyme-linked immunosorbent assay (ELISA). Neat milk from mid-lactating, uninflamed mammary glands (normal milk) effected marked C3 deposition on bacteria. Kinetic studies showed a protracted lag period (30 to 45 min) preceding C3 deposition, which required about 2 h to reach a maximum. Experiments with diluted serum suggested that this slow C3 deposition resulted mainly from the low concentration of certain components of complement in milk. Bacteria incubated in neat milk readily bound bovine conglutinin, indicating the presence of iC3b. Elution of covalently bound C3 fragments with hydroxylamine confirmed the deposition of C3b and iC3b on bacteria. Deposition of C4 on bacteria was not detected in neat milk, suggesting that C3 deposition did not result from the activation of the classical pathway. This was not the result of a lack of antibodies. However, C4 deposition could be obtained by adding purified bovine C1q to normal milk, and C3 deposition was accelerated, suggesting the participation of the classical pathway. The deposition of C1q on antibody-sensitized bacteria was impeded by milk compared with that of C1q diluted in phosphate-buffered saline. Concentrations of C1q in normal milk were very low, ranging from 150 to 250 ng/ml. Overall, these findings indicate that C1q was a limiting factor of the classical pathway in normal milk. The capacity of milk to deposit C3 fragments on mastitis-causing S. agalactiae prompts further studies to investigate its role in opsonophagocytosis.
机译：根据不可检测的溶血活性，通常认为牛乳几乎没有补体，除非炎症吸收血浆成分。这项研究通过酶联免疫吸附试验（ELISA）检查了补体成分在乳腺炎无乳链球菌分离株上的沉积。泌乳中期，未发炎的乳腺的纯牛奶（普通牛奶）在细菌上产生了明显的C3沉积。动力学研究表明，在C3沉积之前有一个较长的延迟期（30至45分钟），需要大约2小时才能达到最大值。用稀释的血清进行的实验表明，这种缓慢的C3沉积主要是由于牛奶中补体某些成分的浓度低所致。在纯牛奶中培养的细菌很容易结合牛凝集素，表明存在iC3b。用羟胺洗脱共价结合的C3片段，证实了C3b和iC3b在细菌上的沉积。在纯牛奶中未检测到细菌上C4的沉积，这表明C3的沉积不是经典途径的激活引起的。这不是缺乏抗体的结果。但是，通过向普通牛奶中添加纯牛C1q可以获得C4沉积，并且C3沉积得以加速，这表明经典途径的参与。与稀释在磷酸盐缓冲液中的C1q相比，牛奶阻碍了C1q在抗体致敏细菌上的沉积。普通牛奶中的C1q浓度非常低，范围从150到250 ng / ml。总体而言，这些发现表明，C1q是正常牛奶中经典途径的限制因素。牛奶在导致乳腺炎的无乳链球菌上沉积C3片段的能力促使人们进行进一步研究，以研究其在调理吞噬作用中的作用。

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