BACKGROUND: Nasal polyposis (NP) is a chronic inflammatory disease often found coexisting with asthma. As this disorder tends to cluster in families, a genetic predisposition has been suggested. Interleukin-1 (IL-1) has been proposed to play a role in the pathogenesis of NP. METHODS: We analysed the single G-to-T base exchange polymorphism in exon 5 at +4845 of the gene encoding IL-1alpha (IL1A) and the C-to-T base exchange polymorphism at -511 of the gene encoding IL-1beta (IL1B) in a population-based sample of adult asthma patients (n = 245). The data were assessed for correlation with data on history of NP and other phenotype-related characteristics. RESULTS: The prevalence of NP in our study group was 14.3%. The distribution of the IL1A genotype differed significantly between asthmatics with and without NP (P = 0.005). The risk of NP was markedly increased in allele G homozygous subjects (OR = 2.73; 95%CI = 1.40-5.32). In the case of IL1B we found no significant associations. Asthmatics with NP had more symptoms than others, but lung function and blood eosinophil counts were similar. CONCLUSIONS: Our study demonstrates an association of IL1A with NP inasthmatic patients and addresses the role of IL-1alpha as an inflammatory modulator in the pathogenesis of this disease.
BACKGROUND:Nasal polyposis (NP) is a chronic inflammatory disease often found coexisting with asthma. As this disorder tends to cluster in families, a genetic predisposition has been suggested. Interleukin-1 (IL-1) has been proposed to play a role in the pathogenesis of NP. METHODS: We analysed the single G-to-T base exchange polymorphism in exon 5 at +4845 of the gene encoding IL-1alpha (IL1A) and the C-to-T base exchange polymorphism at -511 of the gene encoding IL-1beta (IL1B) in a population-based sample of adult asthmapatients (n = 245). The data were assessed for correlation with data on history of NP and other phenotype-related characteristics. RESULTS: The prevalence of NP in our study group was 14.3%. The distribution of the IL1A genotype differed significantly between asthmatics with and without NP (P = 0.005). The risk of NP was markedly increased in allele G homozygous subjects (OR = 2.73; 95%CI = 1.40-5.32). In the case of IL1B we found no significant associations. Asthmatics with NP had more symptoms than others, but lung function and blood eosinophil counts were similar. CONCLUSIONS: Our study demonstrates an association of IL1A with NP inasthmatic patients and addresses the role of IL-1alpha as an inflammatory modulator in the pathogenesis of this disease.
Authors: Joy Hsu; Pedro C Avila; Robert C Kern; M Geoffrey Hayes; Robert P Schleimer; Jayant M Pinto Journal: J Allergy Clin Immunol Date: 2013-04 Impact factor: 10.793
Authors: R A Ramadas; A Sadeghnejad; W Karmaus; S H Arshad; S Matthews; M Huebner; D-Y Kim; S L Ewart Journal: Eur Respir J Date: 2006-11-15 Impact factor: 16.671
Authors: Joel M Bernstein; Jack B Anon; Michael Rontal; Jeffrey Conroy; Chong Wang; Lara Sucheston Journal: Laryngoscope Date: 2009-07 Impact factor: 3.325
Authors: Ramcés Falfán-Valencia; Gandhi F Pavón-Romero; Angel Camarena; María de la Luz García; Gustavo Galicia-Negrete; María Cristina Negrete-García; Luis Manuel Teran Journal: J Allergy (Cairo) Date: 2011-11-03