Asthma is known to run in families, but the genetic mechanisms involved in its pathogenesis are not well understood. The study of thee mechanism requires an understanding of the factors associated with and predisposing to the development of the disease. Several intermediate phenotypes for asthma have been described relating to: total serum IgE levels, bronchial hyperresponsiveness, susceptibility to become sensitized to aeroallergens and baseline airway function (as assessed by spirometry). In addition, segregation analyses have been performed on the families that support the hypothesis that total serum IgE levels are controlled by a major autosomal codominant gene.
The aims of this proposal are: to perform linkage analysis of this putative gene for total IgE levels with candidate genes and with highly polymorphic markers whose location in the human genome is known; and to determine by segregation analysis if a monogenic component is involved in the inheritance of bronchial hyperresponsiveness, baseline airway function, and susceptibility to become sensitized to multiple aeroallergens. These studies will allow a better understanding of the pathogenesis of asthma and help in this prevention and treatment.

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Minority School Faculty Development Awards (K14)
Project #
5K14HL003154-04
Application #
2445008
Study Section
Special Emphasis Panel (ZHL1-CCT-L (F1))
Project Start
1994-08-01
Project End
1999-06-30
Budget Start
1997-07-01
Budget End
1998-06-30
Support Year
4
Fiscal Year
1997
Total Cost
Indirect Cost
Name
University of Arizona
Department
Pediatrics
Type
Schools of Medicine
DUNS #
City
Tucson
State
AZ
Country
United States
Zip Code
85721
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Castro-Rodriguez, J A; Holberg, C J; Wright, A L et al. (1999) Association of radiologically ascertained pneumonia before age 3 yr with asthmalike symptoms and pulmonary function during childhood: a prospective study. Am J Respir Crit Care Med 159:1891-7
Martinez, F D; Holt, P G (1999) Role of microbial burden in aetiology of allergy and asthma. Lancet 354 Suppl 2:SII12-5

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