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首页> 外文期刊>Infection and immunity >Involvement of the Lectin Pathway of Complement Activation in Antimicrobial Immune Defense during Experimental Septic Peritonitis
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Involvement of the Lectin Pathway of Complement Activation in Antimicrobial Immune Defense during Experimental Septic Peritonitis

机译：实验性化脓性腹膜炎过程中补体激活的凝集素途径参与抗菌素免疫防御。

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A critical first line of defense against infection is constituted by the binding of natural antibodies to microbial surfaces, activating the complement system via the classical complement activation pathway. In this function, the classical activation pathway is supported and amplified by two antibody-independent complement activation routes, i.e., the lectin pathway and the alternative pathway. We studied the contribution of the different complement activation pathways in the host defense against experimental polymicrobial peritonitis induced by cecal ligation and puncture by using mice deficient in either C1q or factors B and C2. The C1q-deficient mice lack the classical complement activation pathway. While infection-induced mortality of wild-type mice was 27%, mortality of C1q-deficient mice was increased to 60%. Mice with a deficiency of both factors B and C2 lack complement activation via the classical, the alternative, and the lectin pathways and exhibit a mortality of 92%, indicating a significant contribution of the lectin and alternative pathways of complement activation to survival. For 14 days after infection, mannan-binding lectin (MBL)-dependent activation of C4 was compromised. Serum MBL-A and MBL-C levels were significantly reduced for 1 week, possibly due to consumption. mRNA expression profiles did not lend support for either of the two MBL genes to respond as typical acute-phase genes. Our results demonstrate a long-lasting depletion of MBL-A and MBL-C from serum during microbial infection and underline the importance of both the lectin and the alternative pathways for antimicrobial immune defense.
机译：抵抗感染的关键第一道防线是由天然抗体与微生物表面的结合构成，通过经典的补体激活途径激活补体系统。在这种功能中，经典的激活途径由两条不依赖抗体的补体激活途径，即凝集素途径和替代途径来支持和扩增。我们通过使用缺乏C1q或因子B和C2的小鼠研究了不同补体激活途径在宿主防御盲肠结扎和穿刺引起的实验性微生物腹膜炎中的作用。 C1q缺陷小鼠缺乏经典的补体激活途径。当感染引起的野生型小鼠死亡率为27％时，缺乏C1q的小鼠的死亡率增至60％。缺乏因子B和C2的小鼠缺乏通过经典途径，替代途径和凝集素途径的补体激活，并显示出92％的死亡率，表明凝集素和替代途径的补体激活对存活率的重要贡献。感染后14天，甘露聚糖结合凝集素（MBL）依赖的C4激活受到损害。 1周内，血清MBL-A和MBL-C水平显着降低，可能是由于食用。 mRNA表达谱不支持两个MBL基因之一作为典型的急性期基因做出反应。我们的结果表明，微生物感染期间血清中的MBL-A和MBL-C会长期耗尽，并强调了凝集素和抗微生物免疫防御替代途径的重要性。

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