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Published ahead of print on May 5, 2005, doi:10.1164/rccm.200409-1223OC
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American Journal of Respiratory and Critical Care Medicine Vol 172. pp. 183-188, (2005)
© 2005 American Thoracic Society
doi: 10.1164/rccm.200409-1223OC

Original Article

Positional Identification of an Asthma Susceptibility Gene on Human Chromosome 5q33

Emiko Noguchi, Yukako Yokouchi, Jiang Zhang, Kazuko Shibuya, Akira Shibuya, Makoto Bannai, Katsushi Tokunaga, Hitomi Doi, Mayumi Tamari, Makiko Shimizu, Taro Shirakawa, Masanao Shibasaki, Kunio Ichikawa and Tadao Arinami

Departments of Medical Genetics, Pediatrics, and Immunology, Graduate School of Comprehensive Human Sciences, University of Tsukuba; Department of Pediatrics, Tsukuba College of Technology; Tsukuba Medical Center Hospital, Tsukuba; Department of Human Genetics, Graduate School of Medicine, University of Tokyo, Tokyo; and Laboratory of Genetics of Allergic Diseases, RIKEN SNP Research Center, Yokohama, Japan

Correspondence and requests for reprints should be addressed to Emiko Noguchi, M.D., Ph.D., Department of Medical Genetics, Graduate School of Comprehensive Human Sciences, University of Tsukuba, 1-1-1 Tennoudai, Tsukuba, Ibaraki-ken, 305-8577, Japan. E-mail: enoguchi{at}md.tsukuba.ac.jp

Rationale: Asthma is a common respiratory disease with complex genetic components. We previously reported strong evidence for linkage between mite-sensitive asthma and markers on chromosome 5q33. This area of linkage includes a region homologous to a mouse area that contains a locus involved in regulation of airway hyperreactivity. Objective: The aim of the present study is to identify asthma susceptibility genes on chromosome 5q33. Methods and Results: We performed mutation screening and association analyses of genes in the 9.4-Mb human linkage region. Transmission disequilibrium test analysis of 105 polymorphisms in 155 families with asthma revealed that six polymorphisms in cytoplasmic fragile X mental retardation protein (FMRP)–interacting protein 2 gene were associated significantly with the development of asthma (p = 0.000075; odds ratio, 5.9). These six polymorphisms were in complete linkage disequilibrium. In real-time quantitative polymerase chain reaction analysis, subjects homozygous for the haplotype overtransmitted to asthma-affected offspring showed significantly increased level of cytoplasmic FMRP interacting protein 2 gene expression in lymphocytes compared with ones heterozygous for the haplotype (p = 0.038). Conclusions: Our data suggest that cytoplasmic FMRP interacting protein 2 are associated with the development of atopic asthma in humans, and that targeting cytoplasmic FMRP interacting protein 2 could be a novel strategy for treating atopic asthma.

Key Words: inducible tyrosine kinase • transmission disequilibrium test • polymorphism




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