Atopy and bronchial hyperresponsiveness: Exclusion of linkage to markers on chromosomes 11q and 6p

P. J. Amelung, C. I M Panhuysen, D. S. Postma, Roy C Levitt, G. H. Koeter, C. A. Francomano, E. R. Bleecker, D. A. Meyers

Research output: Contribution to journalArticle

76 Citations (Scopus)

Abstract

Previous studies have reported a familial predisposition for the development of atopy, bronchial hyperresponsiveness and clinical asthma, and therefore have suggested the presence of a heritable component to these disorders. The specific contributions of genetic and environmental factors in the pathogenesis of allergic disease and asthma have not been determined although Cookson et al. [1] have postulated linkage between atopy and chromosome 11q. We have studied 20 families (two and three generations) ascertained through a proband identified as having asthma (90% were also allergic) during the period of time between 1962 and 1970. Of those who were originally skin test positive, 82% remained positive. All probands whose pulmonary function allowed retesting (FEV1 > 1.2 l) remained hyperresponsive to histamine. The children of these probands are now in the same age range as their parents when they were originally evaluated; 66% are atopic using criteria described by Cookson et al. (one or more positive skin tests ≥ 2 mm, an elevated total serum IgE or a positive specific IgE) and 22% demonstrate bronchial hyperresponsiveness (PC20 FEV1) to histamine. Using the highly polymorphic marker INT2 (which maps 2 cM from pλMS.51 on chromosome 11q) and atopy, we obtained a lod score of -2.00 at a recombination fraction of 0.12. In addition, because many studies have suggested an association between atopy and certain HLA antigens, we investigated the possibility of linkage between atopy and bronchial hyperresponsiveness and D6S105, a polymorphic marker on chromosome 6p, located 7 cM from HLA-DR. For this marker and atopy, we observed a lod score of -2.00 with a recombination fraction of 0.07. Similar results were observed with both of these markers and bronchial hyperresponsiveness. By restudying these probands as well as their family members, we were unable to find evidence for linkage between atopy or bronchial hyperresponsiveness and these regions of chromosomes 11 and 6 in this population.

Original languageEnglish
Pages (from-to)1077-1084
Number of pages8
JournalClinical and Experimental Allergy
Volume22
Issue number12
DOIs
StatePublished - Dec 1 1992
Externally publishedYes

Fingerprint

Genetic Markers
Lod Score
Asthma
Skin Tests
Immunoglobulin E
Histamine
Genetic Recombination
Chromosomes
Chromosomes, Human, Pair 11
Chromosomes, Human, Pair 6
HLA-DR Antigens
HLA Antigens
Parents
Lung
Serum
Population

ASJC Scopus subject areas

  • Immunology

Cite this

Amelung, P. J., Panhuysen, C. I. M., Postma, D. S., Levitt, R. C., Koeter, G. H., Francomano, C. A., ... Meyers, D. A. (1992). Atopy and bronchial hyperresponsiveness: Exclusion of linkage to markers on chromosomes 11q and 6p. Clinical and Experimental Allergy, 22(12), 1077-1084. https://doi.org/10.1111/j.1365-2222.1992.tb00133.x

Atopy and bronchial hyperresponsiveness : Exclusion of linkage to markers on chromosomes 11q and 6p. / Amelung, P. J.; Panhuysen, C. I M; Postma, D. S.; Levitt, Roy C; Koeter, G. H.; Francomano, C. A.; Bleecker, E. R.; Meyers, D. A.

In: Clinical and Experimental Allergy, Vol. 22, No. 12, 01.12.1992, p. 1077-1084.

Research output: Contribution to journalArticle

Amelung, PJ, Panhuysen, CIM, Postma, DS, Levitt, RC, Koeter, GH, Francomano, CA, Bleecker, ER & Meyers, DA 1992, 'Atopy and bronchial hyperresponsiveness: Exclusion of linkage to markers on chromosomes 11q and 6p', Clinical and Experimental Allergy, vol. 22, no. 12, pp. 1077-1084. https://doi.org/10.1111/j.1365-2222.1992.tb00133.x
Amelung, P. J. ; Panhuysen, C. I M ; Postma, D. S. ; Levitt, Roy C ; Koeter, G. H. ; Francomano, C. A. ; Bleecker, E. R. ; Meyers, D. A. / Atopy and bronchial hyperresponsiveness : Exclusion of linkage to markers on chromosomes 11q and 6p. In: Clinical and Experimental Allergy. 1992 ; Vol. 22, No. 12. pp. 1077-1084.
@article{64c3107f58c641b788a9cb732a1df658,
title = "Atopy and bronchial hyperresponsiveness: Exclusion of linkage to markers on chromosomes 11q and 6p",
abstract = "Previous studies have reported a familial predisposition for the development of atopy, bronchial hyperresponsiveness and clinical asthma, and therefore have suggested the presence of a heritable component to these disorders. The specific contributions of genetic and environmental factors in the pathogenesis of allergic disease and asthma have not been determined although Cookson et al. [1] have postulated linkage between atopy and chromosome 11q. We have studied 20 families (two and three generations) ascertained through a proband identified as having asthma (90{\%} were also allergic) during the period of time between 1962 and 1970. Of those who were originally skin test positive, 82{\%} remained positive. All probands whose pulmonary function allowed retesting (FEV1 > 1.2 l) remained hyperresponsive to histamine. The children of these probands are now in the same age range as their parents when they were originally evaluated; 66{\%} are atopic using criteria described by Cookson et al. (one or more positive skin tests ≥ 2 mm, an elevated total serum IgE or a positive specific IgE) and 22{\%} demonstrate bronchial hyperresponsiveness (PC20 FEV1) to histamine. Using the highly polymorphic marker INT2 (which maps 2 cM from pλMS.51 on chromosome 11q) and atopy, we obtained a lod score of -2.00 at a recombination fraction of 0.12. In addition, because many studies have suggested an association between atopy and certain HLA antigens, we investigated the possibility of linkage between atopy and bronchial hyperresponsiveness and D6S105, a polymorphic marker on chromosome 6p, located 7 cM from HLA-DR. For this marker and atopy, we observed a lod score of -2.00 with a recombination fraction of 0.07. Similar results were observed with both of these markers and bronchial hyperresponsiveness. By restudying these probands as well as their family members, we were unable to find evidence for linkage between atopy or bronchial hyperresponsiveness and these regions of chromosomes 11 and 6 in this population.",
author = "Amelung, {P. J.} and Panhuysen, {C. I M} and Postma, {D. S.} and Levitt, {Roy C} and Koeter, {G. H.} and Francomano, {C. A.} and Bleecker, {E. R.} and Meyers, {D. A.}",
year = "1992",
month = "12",
day = "1",
doi = "10.1111/j.1365-2222.1992.tb00133.x",
language = "English",
volume = "22",
pages = "1077--1084",
journal = "Clinical and Experimental Allergy",
issn = "0954-7894",
publisher = "Wiley-Blackwell",
number = "12",

}

TY - JOUR

T1 - Atopy and bronchial hyperresponsiveness

T2 - Exclusion of linkage to markers on chromosomes 11q and 6p

AU - Amelung, P. J.

AU - Panhuysen, C. I M

AU - Postma, D. S.

AU - Levitt, Roy C

AU - Koeter, G. H.

AU - Francomano, C. A.

AU - Bleecker, E. R.

AU - Meyers, D. A.

PY - 1992/12/1

Y1 - 1992/12/1

N2 - Previous studies have reported a familial predisposition for the development of atopy, bronchial hyperresponsiveness and clinical asthma, and therefore have suggested the presence of a heritable component to these disorders. The specific contributions of genetic and environmental factors in the pathogenesis of allergic disease and asthma have not been determined although Cookson et al. [1] have postulated linkage between atopy and chromosome 11q. We have studied 20 families (two and three generations) ascertained through a proband identified as having asthma (90% were also allergic) during the period of time between 1962 and 1970. Of those who were originally skin test positive, 82% remained positive. All probands whose pulmonary function allowed retesting (FEV1 > 1.2 l) remained hyperresponsive to histamine. The children of these probands are now in the same age range as their parents when they were originally evaluated; 66% are atopic using criteria described by Cookson et al. (one or more positive skin tests ≥ 2 mm, an elevated total serum IgE or a positive specific IgE) and 22% demonstrate bronchial hyperresponsiveness (PC20 FEV1) to histamine. Using the highly polymorphic marker INT2 (which maps 2 cM from pλMS.51 on chromosome 11q) and atopy, we obtained a lod score of -2.00 at a recombination fraction of 0.12. In addition, because many studies have suggested an association between atopy and certain HLA antigens, we investigated the possibility of linkage between atopy and bronchial hyperresponsiveness and D6S105, a polymorphic marker on chromosome 6p, located 7 cM from HLA-DR. For this marker and atopy, we observed a lod score of -2.00 with a recombination fraction of 0.07. Similar results were observed with both of these markers and bronchial hyperresponsiveness. By restudying these probands as well as their family members, we were unable to find evidence for linkage between atopy or bronchial hyperresponsiveness and these regions of chromosomes 11 and 6 in this population.

AB - Previous studies have reported a familial predisposition for the development of atopy, bronchial hyperresponsiveness and clinical asthma, and therefore have suggested the presence of a heritable component to these disorders. The specific contributions of genetic and environmental factors in the pathogenesis of allergic disease and asthma have not been determined although Cookson et al. [1] have postulated linkage between atopy and chromosome 11q. We have studied 20 families (two and three generations) ascertained through a proband identified as having asthma (90% were also allergic) during the period of time between 1962 and 1970. Of those who were originally skin test positive, 82% remained positive. All probands whose pulmonary function allowed retesting (FEV1 > 1.2 l) remained hyperresponsive to histamine. The children of these probands are now in the same age range as their parents when they were originally evaluated; 66% are atopic using criteria described by Cookson et al. (one or more positive skin tests ≥ 2 mm, an elevated total serum IgE or a positive specific IgE) and 22% demonstrate bronchial hyperresponsiveness (PC20 FEV1) to histamine. Using the highly polymorphic marker INT2 (which maps 2 cM from pλMS.51 on chromosome 11q) and atopy, we obtained a lod score of -2.00 at a recombination fraction of 0.12. In addition, because many studies have suggested an association between atopy and certain HLA antigens, we investigated the possibility of linkage between atopy and bronchial hyperresponsiveness and D6S105, a polymorphic marker on chromosome 6p, located 7 cM from HLA-DR. For this marker and atopy, we observed a lod score of -2.00 with a recombination fraction of 0.07. Similar results were observed with both of these markers and bronchial hyperresponsiveness. By restudying these probands as well as their family members, we were unable to find evidence for linkage between atopy or bronchial hyperresponsiveness and these regions of chromosomes 11 and 6 in this population.

UR - http://www.scopus.com/inward/record.url?scp=0027082077&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0027082077&partnerID=8YFLogxK

U2 - 10.1111/j.1365-2222.1992.tb00133.x

DO - 10.1111/j.1365-2222.1992.tb00133.x

M3 - Article

C2 - 1486537

AN - SCOPUS:0027082077

VL - 22

SP - 1077

EP - 1084

JO - Clinical and Experimental Allergy

JF - Clinical and Experimental Allergy

SN - 0954-7894

IS - 12

ER -