CD46 in meningococcal disease
CD46 in meningococcal disease
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DOI：
10.1126/science.1086476
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发表时间：
2003-07-18
期刊：
影响因子：
56.9
通讯作者：
Jonsson, AB
中科院分区：
文献类型：
--
作者：
Johansson, L;Rytkönen, A;Jonsson, AB
人类特异性细菌病原体脑膜炎奈瑟氏菌是败血症和/或脑膜炎的主要原因。N.脑膜炎与CD 46相互作用，CD 46是一种参与补体激活调节的人细胞表面蛋白。表达人CD 46的转基因小鼠对脑膜炎球菌病易感，因为细菌可以穿过这些小鼠的血脑屏障。疾病的发展是更有效的纤毛细菌鼻内后，但不是腹腔内，挑战的CD 46转基因小鼠，这表明，人CD 46促进纤毛依赖性的相互作用在上皮粘膜。因此，人CD 46转基因小鼠模型是一个潜在的有用的工具，研究发病机制和疫苗的发展，对脑膜炎球菌病。
The human-specific bacterial pathogen Neisseria meningitidis is a major cause of sepsis and/or meningitis. The pili of N. meningitidis interact with CD46, a human cell-surface protein involved in regulation of complement activation. Transgenic mice expressing human CD46 were susceptible to meningococcal disease, because bacteria crossed the blood-brain barrier in these mice. Development of disease was more efficient with piliated bacteria after intranasal, but not intraperitoneal, challenge of CD46 transgenic mice, suggesting that human CD46 facilitates pilus-dependent interactions at the epithelial mucosa. Hence, the human CD46 transgenic mice model is a potentially useful tool for studying pathogenesis and for vaccine development against meningococcal disease.