Deficiency of platelet-activating factor acetylhydrolase is a severity factor for asthma

被引:102
作者
Stafforini, DM
Numao, T
Tsodikov, A
Vaitkus, D
Fukuda, T
Watanabe, N
Fueki, N
McIntyre, TM
Zimmerman, GA
Makino, S
Prescott, SM
机构
[1] Univ Utah, Program Human Mol Biol & Genet, Huntsman Canc Inst, Eccles Inst Human Genet, Salt Lake City, UT 84112 USA
[2] Dokkyo Univ, Sch Med, Dept Med & Clin Immunol, Tochigi, Mibu 3210207, Japan
[3] Jobu NK Hosp, Dept Med, Maebashi, Gunma 3710048, Japan
[4] Univ Utah, Cardiovasc Res & Training Inst, Salt Lake City, UT 84112 USA
关键词
D O I
10.1172/JCI5574
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Asthma, a family of airway disorders characterized by airway inflammation, has an increasing incidence worldwide. Platelet-activating factor (PAF) may play a role in the pathophysiology of asthma. Its proinflammatory actions are antagonized by PAF acetylhydrolase. A missense mutation (V279F) in the PAF acetylhydrolase gene results in the complete loss of activity, which occurs in 4% of the Japanese population. We asked if PAF acetylhydrolase deficiency correlates with the incidence and severity of asthma in Japan. We found that the prevalence of PAF acetylhydrolase deficiency is higher in Japanese asthmatics than healthy subjects and that the severity of this syndrome is highest in homozygous-deficient subjects. We conclude that the PAF acetylhydrolase gene is a modulating locus for the severity of asthma.
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收藏
页码:989 / 997
页数:9
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