REQUIREMENT OF MIP-1-ALPHA FOR AN INFLAMMATORY RESPONSE TO VIRAL-INFECTION

被引:528
作者
COOK, DN
BECK, MA
COFFMAN, TM
KIRBY, SL
SHERIDAN, JF
PRAGNELL, IB
SMITHIES, O
机构
[1] UNIV N CAROLINA, DEPT PEDIAT, CHAPEL HILL, NC 27599 USA
[2] VET AFFAIRS MED CTR, DEPT INTERNAL MED, DURHAM, NC 27710 USA
[3] UNIV N CAROLINA, DEPT MED, CHAPEL HILL, NC 27599 USA
[4] OHIO STATE UNIV, HLTH SCI CTR, DEPT ORAL BIOL, COLUMBUS, OH 43210 USA
[5] OHIO STATE UNIV, HLTH SCI CTR, DEPT MED MICROBIOL & IMMUNOL, COLUMBUS, OH 43210 USA
[6] CRC, BEATSON LABS, GLASGOW G61 1BD, LANARK, SCOTLAND
关键词
D O I
10.1126/science.7667639
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
Macrophage inflammatory protein-1 alpha (MIP-1 alpha) is a chemokine that has pro-inflammatory and stem cell inhibitory activities in vitro. Its biologic role in vivo was examined in mice in which the gene encoding MIP-1 alpha had been disrupted. Homozygous MIP-1 alpha mutant (-/-) mice were resistant to Coxsackievirus-induced myocarditis seen in infected wildtype (+/+) mice. Influenza virus-infected -/- mice had reduced pneumonitis and delayed clearance of the virus compared with infected +/+ mice. The -/- mice had no overt hematopoietic abnormalities. These results demonstrate that MIP-1 alpha is an important mediator of virus-induced inflammation in vivo.
引用
收藏
页码:1583 / 1585
页数:3
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