Department of Medical Genomics, Graduate School of Frontier Sciences, The University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108-8639, Japan.
Exp Parasitol. 2011 Nov;129(3):318-21. doi: 10.1016/j.exppara.2011.07.003. Epub 2011 Jul 13.
It is considered that several glycoproteins on erythrocytes in mammalian species are involved in malaria parasite infection. To elucidate the role of N-glycans on malaria parasite infection, we induced experimental murine malaria infection (using Plasmodium berghei ANKA) in mice deficient in N-acetylglucosaminyltransferase V (Mgat5), which is one of the enzymes involved in β1,6-GlcNAc N-glycan biosynthesis. After infection, Mgat5(-/-) mice showed severe body weight loss and parasitemia compared with wild-type mice. The Mgat5(-/-) mice, but not wild-type mice, also showed severe pathology accompanied by marked infiltration of plasma cells into the lungs and liver. These results suggest that β1,6-GlcNAc N-glycans on/in host erythrocytes may interfere with invasion of the parasites and progression to severe malaria.
据认为，哺乳动物红细胞上的几种糖蛋白参与了疟原虫感染。为了阐明 N-糖链在疟原虫感染中的作用，我们在缺乏 N-乙酰氨基葡萄糖转移酶 V（Mgat5）的小鼠中诱导实验性鼠疟感染（使用 Plasmodium berghei ANKA），Mgat5 是参与β1,6-GlcNAc N-糖链生物合成的酶之一。感染后，与野生型小鼠相比，Mgat5(-/-) 小鼠表现出严重的体重减轻和寄生虫血症。Mgat5(-/-) 小鼠而非野生型小鼠还表现出严重的病理变化，伴有明显的浆细胞浸润到肺部和肝脏。这些结果表明，宿主红细胞上的β1,6-GlcNAc N-糖可能干扰寄生虫的入侵和向严重疟疾的进展。
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