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替代补体途径激活、C反应蛋白与肺炎球菌感染之间的关系。

Relationships between alternative complement pathway activation, C-reactive protein, and pneumococcal infection.

作者信息

Rabinovitch R A, Koethe S M, Kalbfleisch J H, Preheim L C, Rytel M W

出版信息

J Clin Microbiol. 1986 Jan;23(1):56-61. doi: 10.1128/jcm.23.1.56-61.1986.

DOI:10.1128/jcm.23.1.56-61.1986
PMID:3700607
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC268572/
Abstract

In the absence of specific antibody, opsonization of Streptococcus pneumoniae may be mediated by the alternative complement pathway (AP) or by C-reactive protein (CRP) via C1 binding. To determine the role of these mechanisms in pneumococcal (PNC) disease, we studied 19 patients with differing severities of PNC infection. C4 and CRP levels and zymosan-induced consumption of 50% hemolytic complement (CH50) were measured in specimens obtained acutely and then weekly. In patients with complicated illness, the modified mean CH50 in acute sera was 178 +/- 57 U/ml, significantly lower than the mean CH50 of 331 +/- 80 U/ml in patients with uncomplicated illness (P less than 0.05). The values of the two groups on a given day approximated each other on days 7, 14, and 23. Consumption of complement by zymosan was also lower in acute sera of patients with complicated illness, with a mean value of 19 +/- 18 U/ml compared with 58 +/- 30 U/ml in those with uncomplicated illness (P less than 0.05). This difference was also seen on day 7 (P less than 0.05). Disease involving lower-numbered PNC serotypes (less than 10) correlated with reduced availability of AP factors in acute sera, independent of illness severity. Mean CRP levels were inversely related to zymosan-induced complement activation in patients with complicated illness. These data suggest that in vivo depletion of AP factors is significantly greater in patients with complicated illness and is associated with high CRP levels. CRP may enhance AP activation via C3 convertase generation and function with it as a preantibody host defense mechanism.

摘要

在缺乏特异性抗体的情况下,肺炎链球菌的调理作用可能由替代补体途径(AP)介导,或由C反应蛋白(CRP)通过C1结合介导。为了确定这些机制在肺炎球菌(PNC)疾病中的作用,我们研究了19例不同严重程度的PNC感染患者。在急性期及之后每周采集的标本中检测C4和CRP水平以及酵母聚糖诱导的50%溶血补体(CH50)消耗情况。在患有复杂疾病的患者中,急性血清中改良平均CH50为178±57 U/ml,显著低于非复杂疾病患者的平均CH50 331±80 U/ml(P<0.05)。两组在第7天、14天和23天的给定日期的值相互接近。患有复杂疾病患者的急性血清中酵母聚糖介导的补体消耗也较低,平均值为19±18 U/ml,而无复杂疾病患者为58±30 U/ml(P<0.05)。在第7天也观察到了这种差异(P<0.05)。涉及较低编号PNC血清型(少于10种)的疾病与急性血清中AP因子可用性降低相关,与疾病严重程度无关。在患有复杂疾病的患者中,平均CRP水平与酵母聚糖诱导的补体激活呈负相关。这些数据表明,患有复杂疾病的患者体内AP因子的消耗明显更大,且与高CRP水平相关。CRP可能通过生成C3转化酶增强AP激活,并与之共同作为一种前抗体宿主防御机制发挥作用。

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本文引用的文献

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PNEUMOCOCCAL BACTEREMIA WITH ESPECIAL REFERENCE TO BACTEREMIC PNEUMOCOCCAL PNEUMONIA.肺炎球菌血症,特别是关于菌血症性肺炎球菌肺炎
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Activation of C3 via the alternative complement pathway results in fixation of C3b to the pneumococcal cell wall.通过替代补体途径激活C3会导致C3b固定在肺炎球菌细胞壁上。
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The fixation of C3b to pneumococcal cell wall polymers as a result of activation of the alternative complement pathway.由于替代补体途径的激活,C3b固定于肺炎球菌细胞壁聚合物上。
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Inhibitory effect of C-reactive protein on alternative C pathway activation by liposomes and Streptococcus pneumoniae.C反应蛋白对脂质体和肺炎链球菌激活补体替代途径的抑制作用。
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Heat labile opsonins to Pneumococcus. 3. The participation of immunoglobulin and of the alternate pathway of C3 activation.对肺炎球菌的热不稳定调理素。3. 免疫球蛋白和补体C3激活替代途径的参与。
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