Data di Pubblicazione:
2009
Abstract:
Obesity is a risk factor for asthma. Adipose tissue expresses pro-inflammatory molecules including tumour necrosis factor (TNF), and levels of TNF are also related to polymorphisms in the TNF-a (TNFA) gene. The current authors examined the joint effect of obesity and TNFA variability on asthma in adults by combining two population-based studies. The European Community Respiratory Health Survey and the Swiss Cohort Study on Air
Pollution and Lung and Heart Disease in Adults used comparable protocols, questionnaires and measures of lung function and atopy. DNA samples from 9,167 participants were genotyped for TNFA -308 and lymphotoxin-a (LTA) +252 gene variants. Obesity and TNFA were associated with asthma when mutually adjusting for their independent effects (odds ratio (OR) for obesity 2.4, 95% confidence interval (CI) 1.7–3.2; OR for TNFA -308
polymorphism 1.3, 95% CI 1.1–1.6). The association of obesity with asthma was stronger for subjects carrying the G/A and A/A TNFA -308 genotypes compared with the more common G/G genotype, particularly among nonatopics (OR for G/A and A/A genotypes 6.1, 95% CI 2.5–14.4; OR for G/G genotype 1.7, 95% CI 0.8–3.3). The present findings provide, for the first time, evidence for a complex pattern of interaction between obesity, a pro-inflammatory genetic factor and asthma.
Pollution and Lung and Heart Disease in Adults used comparable protocols, questionnaires and measures of lung function and atopy. DNA samples from 9,167 participants were genotyped for TNFA -308 and lymphotoxin-a (LTA) +252 gene variants. Obesity and TNFA were associated with asthma when mutually adjusting for their independent effects (odds ratio (OR) for obesity 2.4, 95% confidence interval (CI) 1.7–3.2; OR for TNFA -308
polymorphism 1.3, 95% CI 1.1–1.6). The association of obesity with asthma was stronger for subjects carrying the G/A and A/A TNFA -308 genotypes compared with the more common G/G genotype, particularly among nonatopics (OR for G/A and A/A genotypes 6.1, 95% CI 2.5–14.4; OR for G/G genotype 1.7, 95% CI 0.8–3.3). The present findings provide, for the first time, evidence for a complex pattern of interaction between obesity, a pro-inflammatory genetic factor and asthma.
Tipologia CRIS:
1.1 Articolo in rivista
Keywords:
Asthma; Atopy; Genetic polymorphism; Obesity; Tumour necrosis factor-a; Adult; Alleles; Asthma; Chi-Square Distribution; Cohort Studies; Europe; Female; Genotype; Humans; Logistic Models; Male; Obesity; Research Design; Respiratory Function Tests; Risk Factors; Surveys and Questionnaires; Switzerland; Tumor Necrosis Factor-alpha; Polymorphism, Single Nucleotide; Medicine (all); Pulmonary and Respiratory Medicine
Elenco autori:
Castro Giner, F.; Kogevinas, M.; Imboden, M.; de Cid, R.; Jarvis, D.; Mächler, M.; Berger, W.; Burney, P.; Franklin, K. A.; Gonzalez, J. R.; Heinrich, J.; Janson, C.; Omenaas, E.; Pin, I.; Rochat, T.; Sunyer, J.; Wjst, M.; Antó, J. M.; Estivill, X.; Probst Hensch, N. M.; Broglie, M.; Bünter, M.; Gashi, D.; Armbruster, R.; Damm, T.; Egermann, U.; Gut, M.; Maier, L.; Vögelin, A.; Walter, L.; Jud, D.; Lutz, N.; Ares, M.; Bennour, M.; Galobardes, B.; Namer, E.; Baumberger, B.; Boccia Soldati, S.; Gehrig Van Essen, E.; Ronchetto, S.; Bonvin, C.; Burrus, C.; Blanc, S.; Ebinger, A. V.; Fragnière, M. L.; Jordan, J.; Gimmi, R.; Kourkoulos, N.; Schafroth, U.; Bauer, N.; Baehler, D.; Gabriel, C.; Nilly, R.; Ackermann Liebrich, U.; Gaspoz, J. M.; Leuenberger, P.; Liu, L. J. S.; Schindler, C.; Barthélémy, J. C.; Bettschart, R.; Bircher, A.; Bolognini, G.; Brändli, O.; Brutsche, M.; Burdet, L.; Frey, M.; Gerbase, M. W.; Gold, D.; Karrer, W.; Keller, R.; Knöpfli, B.; Künzli, N.; Neu, U.; Nicod, L.; Pons, M.; Russi, E.; Schmid Grendelmeyer, P.; Schwartz, J.; Straehl, P.; Tschopp, J. M.; von Eckardstein, A.; Zellweger, J. P.; Zemp Stutz, E.; Bridevaux, P. O.; Curjuric, I.; Downs, S. H.; Felber Dietrich, D.; Gemperli, A.; Keidel, D.; Imboden, M.; Staedele Kessler, P.; Thun, G. A.; Abramson, M.; Woods, R.; Walters, E. H.; Thien, F.; Benke, G.; Vermeire, P.; Weyler, J.; Van Sprundel, M.; Nelen, V.; Jogi, R.; Soon, A.; Neukirch, F.; Leynaert, B.; Liard, R.; Zureik, M.; Pin, I.; Ferran Quentin, J.; Heinrich, J.; Frye, C.; Meyer, I.; Gislason, T.; Bugiani, M.; Piccioni, P.; Carosso, A.; Arossa, W.; Caria, E.; Castiglioni, G.; Migliore, E.; Romano, C.; Fabbro, D.; Ciccone, G.; Magnani, C.; Dalmasso, P.; Bono, R.; Gigli, G.; Giraudo, A.; Brussino, M. C.; Bucca, C.; Rolla, G.; de Marco, R.; Verlato, G.; Zanolin, E.; Accordini, S.; Poli, A.; Lo Cascio, V.; Ferrari, M.; Marinoni, A.; Villani, S.; Ponzio, M.; Frigerio, F.; Comelli, M.; Grassi, Mario; Cerveri, I.; Corsico, ANGELO GUIDO; Schouten, J.; Gulsvik, A.; Svanes, C.; Laerum, B.; Zock, J. P.; Basagana, X.; Jaen, A.; Burgos, F.; Maldonado, J.; Pereira, A.; Sanchez, J. L.; Martinez Moratalla Rovira, J.; Almar, E.; Muniozguren, N.; Urritia, I.; Payo, F.; Janson, C.; Boman, G.; Norback, D.; Gunnbjornsdottir, M.; Toren, K.; Lillienberg, L.; Dahlman Höglund, A.; Sundberg, R.; Norrman, E.; Soderberg, M.; Franklin, K. A.; Lundback, B.; Forsberg, B.; Nystrom, L.; Dibbert, B.; Hazenkamp, M.; Brutsche, M.; Burney, P.; Chinn, S.; Harrison, B.; Jarvis, D.; Hall, R.; Seaton, D.; Osborne, M.; Buist, S.; Vollmer, W.; Johnson, L.
Link alla scheda completa:
Pubblicato in: