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Published ahead of print on March 12, 2004, doi:10.1164/rccm.200302-281OC
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American Journal of Respiratory and Critical Care Medicine Vol 169. pp. 1217-1223, (2004)
© 2004 American Thoracic Society

Original Article

Association of the Interleukin-1 Receptor Antagonist Gene with Asthma

Henning Gohlke, Thomas Illig, Margret Bahnweg, Norman Klopp, Elisabeth André, Janine Altmüller, Nicole Herbon, Monika Werner, Michael Knapp, Lydia Pescollderungg, Attilio Boner, Giovanni Malerba, Pier Franco Pignatti and Matthias Wjst

GSF-National Research Center for Environment and Health, Institute of Epidemiology, Neuherberg; Institute for Medical Biometry, Informatics, and Epidemiology, University of Bonn, Bonn, Germany; Department of Pediatrics, Bolzano Hospital, Bolzano; and Department of Mother and Child, Biology and Genetics, University of Verona, Verona, Italy

Correspondence and requests for reprints should be addressed to Matthias Wjst, M.D., GSF-National Research Center for Environment and Health, Institute of Epidemiology, Ingolstaedter Landstraße 1, D-85764 Neuherberg, Germany. E-mail: m{at}wjst.de

The interleukin-1 cluster on human chromosome 2q12-2q14 harbors various promising candidate genes for asthma and other inflammatory diseases. We conducted a systematic association study with single-nucleotide polymorphisms (SNPs) located in candidate genes situated in this cluster. Single-marker, two-locus and three-locus haplotype analysis of SNPs yielded several significant results (p < 0.05–0.0021) for the human IL1RN gene encoding the IL-1 receptor antagonist protein, an antiinflammatory cytokine that plays an important role in maintaining the balance between inflammatory and antiinflammatory cytokines. These findings were replicated and confirmed in an independent Italian family sample in which significant, although weaker, association with asthma was detected. A sequencing approach to the coding region of the human IL1RN gene revealed additional DNA variants, from which a selection was also associated with the disease in German and Italian samples. Calculation of the linkage disequilibrium for the human IL1RN gene showed strong linkage disequilibrium for nearly all analyzed SNPs. Further haplotype analysis indicated that six SNPs are sufficient for tagging all haplotypes with a prevalence of more than 1%. The most frequent haplotype constructed from these SNPs was 1.4-fold overtransmitted in the German family sample.

Key Words: association • asthma • IL1RN • single-nucleotide polymorphisms




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