A genome-wide linkage analysis of orchard grass-sensitive childhood seasonal allergic rhinitis in Japanese families

被引:42
作者
Yokouchi, Y
Shibasaki, M
Noguchi, E
Nakayama, J
Ohtsuki, T
Kamioka, M
Yamakawa-Kobayashi, K
Ito, S
Takeda, K
Ichikawa, K
Nukaga, Y
Matsui, A
Hamaguchi, H
Arinami, T [1 ]
机构
[1] Univ Tsukuba, Inst Basic Med Sci, Dept Med Genet, Tsukuba, Ibaraki 3058575, Japan
[2] Univ Tsukuba, Inst Clin Med, Dept Pediat, Tsukuba, Ibaraki, Japan
[3] Univ Tsukuba, Dept Dermatol, Tsukuba, Ibaraki, Japan
关键词
seasonal allergic rhinitis; multipoint linkage; genome-wide scan; orchard grass;
D O I
10.1038/sj.gene.6363815
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
Seasonal allergic rhinitis (SAR) is an inflammatory disease of the nose and eyes that follows sensitization to air-born pollens. We conducted a genome-wide linkage screening of 48 Japanese families (188 members) with orchard grass (OG)-sensitive SAR children (67 affected sib-pairs) in a farming community in central Japan where OG was planted for apple farming and OG pollen is a major cause of SAR. We used the GENEHUNTER program to performed nonparametric multipoint linkage analysis for OG-sensitive SAR as a qualitative trait and for log total serum IgE levels and OG-RAST IgE levels as quantitative traits. Genotyping data of 400 microsatellite markers suggested linkage of SAR to chromosomes 1p36.2, 4q13.3, and 9q34.3 (P < 0.001), linkage of serum total IgE levels to 3p24.1, 5q33.1, 12p13.1, and 12q24.2 (P < 0.001), and linkage of OG-RAST IgE levels to 4p16.1, 11q14.3, and 16p12.3 (P < 0.001). Weak evidence for linkage of SAR to 5q33.1 was also observed (P = 0.01). All these regions, with the exception of 9q34.3, have been previously reported to be linked to asthma and/or atopy. These data suggest that, although loci linked to SAR are likely to be common to asthma, a strong contribution by specific gene(s) to OG-sensitive SAR is unlikely.
引用
收藏
页码:9 / 13
页数:5
相关论文
共 34 条
[1]   EVIDENCE FOR LINKAGE OF TOTAL SERUM IGE AND BRONCHIAL HYPERRESPONSIVENESS TO CHROMOSOME 5Q - A MAJOR REGULATORY LOCUS IMPORTANT IN ASTHMA [J].
BLEECKER, ER ;
AMELUNG, PJ ;
LEVITT, RC ;
POSTMA, DS ;
MEYERS, DA .
CLINICAL AND EXPERIMENTAL ALLERGY, 1995, 25 :84-88
[2]  
BLUMENTHAL M, 1992, J IMMUNOL, V148, P411
[3]  
BORECKI I B, 1985, Genetic Epidemiology, V2, P327, DOI 10.1002/gepi.1370020402
[4]   A genome-wide search for quantitative trait loci underlying asthma [J].
Daniels, SE ;
Bhattacharrya, S ;
James, A ;
Leaves, NI ;
Young, A ;
Hill, MR ;
Faux, JA ;
Ryan, GF ;
leSouef, PN ;
Lathrop, GM ;
Musk, AW ;
Cookson, WOCM .
NATURE, 1996, 383 (6597) :247-250
[5]   The natural course of allergic rhinitis during 12 years of follow-up [J].
Danielsson, J ;
Jenssen, M .
ALLERGY, 1997, 52 (03) :331-334
[6]  
Deichmann KA, 1998, CLIN EXP ALLERGY, V28, P151
[7]   DETECTION OF A RECESSIVE MAJOR GENE FOR HIGH IGE LEVELS ACTING INDEPENDENTLY OF SPECIFIC RESPONSE TO ALLERGENS [J].
DIZIER, MH ;
HILL, M ;
JAMES, A ;
FAUX, J ;
RYAN, G ;
LESOUEF, P ;
LATHROP, M ;
MUSK, AW ;
DEMENAIS, F ;
COOKSON, W .
GENETIC EPIDEMIOLOGY, 1995, 12 (01) :93-105
[8]   Co-existence of asthma and allergic rhinitis: A 23-year follow-up study of college students [J].
Greisner, WA ;
Settipane, RJ ;
Settipane, GA .
ALLERGY AND ASTHMA PROCEEDINGS, 1998, 19 (04) :185-188
[9]   Genetic linkage of hyper-IgE syndrome to chromosome 4 [J].
Grimbacher, B ;
Schäffer, AA ;
Holland, SM ;
Davis, J ;
Gallin, JI ;
Malech, HL ;
Atkinson, TP ;
Belohradsky, BH ;
Buckley, RH ;
Cossu, F ;
Español, T ;
Garty, BZ ;
Matamoros, N ;
Myers, LA ;
Nelson, RP ;
Ochs, HD ;
Renner, ED ;
Wellinghausen, N ;
Puck, JM .
AMERICAN JOURNAL OF HUMAN GENETICS, 1999, 65 (03) :735-744
[10]   Linkage analysis of Dermatophagoides pteronyssinus-specific IgE responsiveness with polymorphic markers on chromosome 6p21 (HLA-D region) in Caucasian families by the transmission/disequilibrium test [J].
Hizawa, N ;
Collins, G ;
Rafnar, T ;
Huang, SK ;
Duffy, DL ;
Weber, JL ;
Freidhoff, LR ;
Ehrlich, E ;
Marsh, DG ;
Beaty, TH ;
Barnes, KC .
JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, 1998, 102 (03) :443-448