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首页> 外文期刊>Infection and immunity >Mannose-Binding Lectin Is a Disease Modifier in Clinical Malaria and May Function as Opsonin for Plasmodium falciparum- Infected Erythrocytes
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Mannose-Binding Lectin Is a Disease Modifier in Clinical Malaria and May Function as Opsonin for Plasmodium falciparum- Infected Erythrocytes

机译：结合有甘露糖的凝集素是临床疟疾的疾病改良剂，可能充当恶性疟原虫感染的红细胞的调理素

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Variant alleles in the mannose-binding lectin (MBL) gene (mbl2) causing low levels of functional MBL are associated with susceptibility to different infections and are common in areas where malaria is endemic. Therefore, we investigated whether MBL variant alleles in 551 children from Ghana were associated with the occurrence and outcome parameters of Plasmodium falciparum malaria and asked whether MBL may function as an opsonin for P. falciparum. No difference in MBL genotype frequency was observed between infected and noninfected children or between children with cerebral malaria and/or severe malarial anemia and children with uncomplicated malaria. However, patients with complicated malaria who were homozygous for MBL variant alleles had significantly higher parasite counts and lower blood glucose levels than their MBL-competent counterparts. Distinct calcium-dependent binding of MBL to the membrane of P. falciparum-infected erythrocytes, which could be inhibited by mannose, was observed. Further characterization revealed that MBL reacted with a P. falciparum glycoprotein identical to the 78-kDa glucose-regulated stress protein of P. falciparum. MBL seems to be a disease modifier in clinical malaria and to function as an opsonin for erythrocytes invaded by P. falciparum and may thus be involved in sequestration of the parasite, which in turn may explain the association between homozygosity for MBL variant alleles and high parasite counts.
机译：导致低水平功能性MBL的甘露糖结合凝集素（MBL）基因（ mbl2 ）中的变异等位基因与不同感染的易感性有关，在疟疾流行地区很常见。因此，我们调查了551名来自加纳的儿童的MBL变异等位基因是否与恶性疟原虫疟疾的发生和结局相关，并询问MBL是否可作为 P的调理素。恶心。在感染和未感染的儿童之间，或在患有脑疟疾和/或严重疟疾贫血的儿童与没有并发症的疟疾儿童之间，未观察到MBL基因型频率的差异。然而，与MBL对应的同伴相比，MBL变异等位基因纯合的复杂疟疾患者的寄生虫计数显着更高，血糖水平更低。钙依赖的MBL与 P膜的独特结合。观察到被甘露糖抑制的恶性疟原虫感染的红细胞。进一步表征表明，MBL与 P反应。恶性疟原虫糖蛋白与78 kDa葡萄糖调节的 P应激蛋白相同。恶心。 MBL在临床疟疾中似乎是一种疾病改良剂，并且对 P侵袭的红细胞起调理素的作用。恶性疟原虫，因此可能参与了寄生虫的隔离，这反过来可以解释MBL变异等位基因的纯合性与高寄生虫计数之间的关联。

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