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Genetic Analysis of Antigen-Induced Airway Manifestations of Asthma Using Recombinant Congenic Mouse Strains*

Antoon J.M. Van Oosterhout, PhD; Prescilla V. Jeurink; Peter C. Groot, PhD; Gerard A. Hofman; Frans P. Nijkamp, PhD; Peter Demant, PhD
Author and Funding Information

*From the Department of Pharmacology and Pathophysiology (Drs. Van Oosterhout, Groot, and Nijkamp, Ms. Jeurink, and Mr. Hofman), Faculty of Pharmacy, Utrecht University, Utrecht, Netherlands; Division of Molecular Genetics (Dr. Demant), Netherlands Cancer Institute, Amsterdam, Netherlands.

Correspondence to: Antoon J.M. Van Oosterhout, PhD, Department of Pharmacology and Pathophysiology, Faculty of Pharmacy, Utrecht University, PO box 80.082, 3508TB Utrecht, Netherlands; e-mail: a.j.m.vanoosterhout@pharm.uu.nl



Chest. 2002;121(3_suppl):13S. doi:10.1378/chest.121.3_suppl.13S
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Allergic asthma is a heterogeneous and genetically complex disease that is characterized by the presence of allergen-specific IgE, eosinophilic airway inflammation, and hyperresponsiveness to bronchospasmogenic stimuli. To facilitate the mapping of genes controlling complex asthma traits, we have used a powerful tool, the recombinant congenic strains of mice, which transforms a multigenic difference into a set of monogenic or oligogenic differences.1 This approach offers a higher resolution power than do the standard mouse crosses in mapping segregating quantitative trait loci and in the detection of their potential interactions. In the present study, we compared 4 strains (Ccs/DEM-5, Ccs/DEM-11, Ccs/DEM-12, and Ccs/DEM-18) from a series of 20 strains, each of which carries a random set of 12.5% of genes from the T-helper cell type 1 responder strain STS and 87.5% of genes from the T-helper cell type 2 responder strain BALB/c. Mice were sensitized with ovalbumin (OVA), and later on were repeatedly challenged by the inhalation of an OVA aerosol. Before and after the OVA challenges, serum samples were obtained and the airway responsiveness to nebulized methacholine (dose range, 1.5 to 50 mg/mL) was determined. Finally, BAL was performed, and the number of leukocytes were determined (Table 1 ).

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