Table of Contents
Journal of Allergy
Volume 2012, Article ID 741313, 5 pages
http://dx.doi.org/10.1155/2012/741313
Research Article

The IL1B-511 Polymorphism (rs16944 AA Genotype) Is Increased in Aspirin-Exacerbated Respiratory Disease in Mexican Population

HLA Laboratory, Department of Immunogenetics and Allergy, Instituto Nacional de Enfermedades Respiratorias, Tlalpan 4502, Sección XVI, Delegación Tlalpan, 14080 México, DF, Mexico

Received 2 July 2011; Revised 16 September 2011; Accepted 16 September 2011

Academic Editor: A. P. Sampson

Copyright © 2012 Ramcés Falfán-Valencia et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Aspirin exacerbated respiratory disease (AERD) is characterized by chronic hyperplastic rhinosinusitis, nasal polyposis, asthma, and aspirin sensitivity. The mechanisms which produce these manifestations of intolerance are not fully defined, current research focuses on cyclooxygenase 1 (COX-1) inhibition, metabolism of arachidonic acid, and the COX pathway to the lipoxygenase (LO) route, inducing increased synthesis of leukotrienes (LT). The biological plausibility of this model has led to the search for polymorphisms in genes responsible for proinflammatory cytokines synthesis, such as IL1B and IL8. We performed a genetic association study between IL8-251 (rs4073) and IL1B-511 (rs16944) polymorphisms in AERD, aspirin-tolerant asthma (ATA), and healthy control subjects. Using allelic discrimination by real-time PCR, we found statistically nonsignificant associations between AERD, ATA, and healthy control subjects for the GG and GA genotypes of IL1B (rs16944). Interestingly, the AA genotype showed an increased frequency in the AERD patients versus the ATA group (GF = 0.19 versus 0.07, 𝑝 = 0 . 0 1 8 , OR 2.98, and 95% CI 1.17–7.82). This is the first observation that IL1B polymorphisms are involved in AERD. Thus, future studies must investigate whether interleukin-1 𝛽 is released in the airways of AERD patients and whether it relates to genetic polymorphisms in the IL1B gene.