甘露聚糖结合蛋白与补体依赖性调节在酒精性肝硬化中的作用。

C Homann, P Garred, P Hasselqvist, N Graudal, S Thiel, A C Thomsen
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引用次数: 20

摘要

甘露聚糖结合蛋白是由肝脏合成的,通过激活经典补体途径(不依赖于Clq),调理富含甘露聚糖的微生物,并通过其固有的调理和介导吞噬的能力,在一线宿主防御中发挥作用。我们研究了肝硬化患者对细菌感染的易感性增加是否可以通过低血浆甘露聚糖结合蛋白浓度和补体依赖性调理受损来解释。我们检查了51例代偿性酒精性肝硬化患者,34例失代偿性肝硬化患者和16例健康对照。无论在哪个组,我们发现血浆甘露聚糖结合蛋白浓度与面包酵母甘露聚糖上补体调理素C4的沉积显著相关(p < 0.05)。与预期相反,失代偿期肝硬化患者的这种调理和血浆甘露聚糖结合蛋白水平显著升高(p = 0.01和p = 0.007)。甘露聚糖结合蛋白与这些患者的红细胞沉降率、纤维蛋白原和接触珠蛋白之间存在显著相关(0 < 0.05)。尽管相关性较弱(rho分别为0.49、0.48和0.40),失代偿期肝硬化患者甘露聚糖结合蛋白水平升高可能反映急性期反应。结论:失代偿肝硬化患者血浆甘露聚糖结合蛋白水平升高,而酒精性肝硬化患者甘露聚糖的补体依赖性调理似乎没有受到损害。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Mannan-binding protein and complement dependent opsonization in alcoholic cirrhosis.

Mannan-binding protein is synthesized by the liver and functions in first-line host defence by opsonizing mannose-rich microorganisms due to activation of the classical complement pathway independent of Clq, and by an intrinsic ability to opsonize and mediate phagocytosis. We have investigated whether the increased susceptibility to bacterial infections in patients with cirrhosis could be explained by low plasma concentrations of mannan-binding protein and impaired complement-dependent opsonization. We examined 51 patients with compensated alcoholic cirrhosis, 34 who were decompensated and 16 healthy controls. Irrespective of group, we found a significant correlation (p < 0.05) between plasma mannan-binding protein concentration and deposition of the complement opsonin C4 on mannan from baker's yeast. In contrast to what was expected, this kind of opsonization and plasma levels of mannan-binding protein were significantly increased in the patients with decompensated cirrhosis (p = 0.01 and p = 0.007, respectively). A significant correlation (0 < 0.05) was found between mannan-binding protein and erythrocyte sedimentation rate, fibrinogen and haptoglobin in these patients. Though the correlations were weak (rho = 0.49, rho = 0.48 and rho = 0.40, respectively), the elevated levels of mannan-binding protein in the patients with decompensated cirrhosis may reflect an acute phase reaction. It is concluded that plasma levels of mannan-binding protein are increased in patients with decompensated cirrhosis and that complement-dependent opsonization of mannan does not seem to be compromized in patients with alcoholic cirrhosis.

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