CD46 in meningococcal disease

被引:126
作者
Johansson, L
Rytkönen, A
Bergman, P
Albiger, B
Källström, H
Hökfelt, T
Agerberth, B
Cattaneo, R
Jonsson, AB
机构
[1] Ctr Microbiol & Tumor Biol, SE-17177 Stockholm, Sweden
[2] Karolinska Inst, Dept Med Biochem & Biophys, SE-17177 Stockholm, Sweden
[3] Karolinska Inst, Dept Cell & Mol Biol, SE-17177 Stockholm, Sweden
[4] Karolinska Inst, Dept Neurosci, SE-17177 Stockholm, Sweden
[5] Swedish Inst Infect Dis Control, SE-17182 Solna, Sweden
[6] Mayo Clin & Mayo Fdn, Program Mol Med, Rochester, MN 55905 USA
关键词
D O I
10.1126/science.1086476
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
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.
引用
收藏
页码:373 / 375
页数:3
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