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

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) inhib...

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Autores principales: Falfán-Valencia, Ramcés, Pavón-Romero, Gandhi F., Camarena, Angel, García, María de la Luz, Galicia-Negrete, Gustavo, Negrete-García, María Cristina, Teran, Luis Manuel
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3216272/
https://www.ncbi.nlm.nih.gov/pubmed/22132000
http://dx.doi.org/10.1155/2012/741313
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author Falfán-Valencia, Ramcés
Pavón-Romero, Gandhi F.
Camarena, Angel
García, María de la Luz
Galicia-Negrete, Gustavo
Negrete-García, María Cristina
Teran, Luis Manuel
author_facet Falfán-Valencia, Ramcés
Pavón-Romero, Gandhi F.
Camarena, Angel
García, María de la Luz
Galicia-Negrete, Gustavo
Negrete-García, María Cristina
Teran, Luis Manuel
author_sort Falfán-Valencia, Ramcés
collection PubMed
description 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 = 0.018, 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-1β is released in the airways of AERD patients and whether it relates to genetic polymorphisms in the IL1B gene.
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spelling pubmed-32162722011-11-30 The IL1B-511 Polymorphism (rs16944 AA Genotype) Is Increased in Aspirin-Exacerbated Respiratory Disease in Mexican Population Falfán-Valencia, Ramcés Pavón-Romero, Gandhi F. Camarena, Angel García, María de la Luz Galicia-Negrete, Gustavo Negrete-García, María Cristina Teran, Luis Manuel J Allergy (Cairo) Research Article 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 = 0.018, 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-1β is released in the airways of AERD patients and whether it relates to genetic polymorphisms in the IL1B gene. Hindawi Publishing Corporation 2012 2011-11-03 /pmc/articles/PMC3216272/ /pubmed/22132000 http://dx.doi.org/10.1155/2012/741313 Text en Copyright © 2012 Ramcés Falfán-Valencia et al. https://creativecommons.org/licenses/by/3.0/ 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.
spellingShingle Research Article
Falfán-Valencia, Ramcés
Pavón-Romero, Gandhi F.
Camarena, Angel
García, María de la Luz
Galicia-Negrete, Gustavo
Negrete-García, María Cristina
Teran, Luis Manuel
The IL1B-511 Polymorphism (rs16944 AA Genotype) Is Increased in Aspirin-Exacerbated Respiratory Disease in Mexican Population
title The IL1B-511 Polymorphism (rs16944 AA Genotype) Is Increased in Aspirin-Exacerbated Respiratory Disease in Mexican Population
title_full The IL1B-511 Polymorphism (rs16944 AA Genotype) Is Increased in Aspirin-Exacerbated Respiratory Disease in Mexican Population
title_fullStr The IL1B-511 Polymorphism (rs16944 AA Genotype) Is Increased in Aspirin-Exacerbated Respiratory Disease in Mexican Population
title_full_unstemmed The IL1B-511 Polymorphism (rs16944 AA Genotype) Is Increased in Aspirin-Exacerbated Respiratory Disease in Mexican Population
title_short The IL1B-511 Polymorphism (rs16944 AA Genotype) Is Increased in Aspirin-Exacerbated Respiratory Disease in Mexican Population
title_sort il1b-511 polymorphism (rs16944 aa genotype) is increased in aspirin-exacerbated respiratory disease in mexican population
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3216272/
https://www.ncbi.nlm.nih.gov/pubmed/22132000
http://dx.doi.org/10.1155/2012/741313
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