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.

Joint effect of obesity and TNFA variability on asthma: two international cohort studies

ROMANO, Canzio;BONO, Roberto;BRUSSINO, Luisa;BUCCA, Caterina;ROLLA, Giovanni;
2009-01-01

Abstract

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.
2009
33
5
1003
1009
OBESITY; ASTHMA; TUMOR NECROSIS FACTOR
Castro-Giner F; Kogevinas M; Imboden M; de Cid R; Jarvis D; Machler M; Berger W; Burney P; Franklin KA; Gonzalez JR; Heinrich J; Janson C; Omenaas E; Pin I; Rochat T; Sunyer J; Wjst M; Anto´ J-M; Estivill X and Probst-Hensch NM. The ECRHS list of principal investigators and the senior scientific team are as follows: Melbourne; Australia: Abramson M; Woods R; Walters EH; Thien F and Benke G. South Antwerp and Antwerp City; Belgium: Vermeire P; Weyler J; Van Sprundel M and Nelen V. Tartu; Estonia: Jogi R and Soon A. Paris;France: Neukirch F; Leynaert B; Liard R and Zureik M. Grenoble; France: Pin I; Ferran-Quentin J. Erfurt; Germany: Heinrich J; Wjst M; Frye C and Meyer I. Reykjavik; Iceland: Gislason T. Turin; Italy: 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 MC; Bucca C; Rolla G. Verona; Italy: de Marco R; Verlato G; Zanolin E; Accordini S; Poli A; Lo Cascio V and Ferrari M. Pavia; Italy: Marinoni A; Villani S; Ponzio M; Frigerio F; Comelli M; Grassi M; Cerveri I and Corsico A. Groningen; the Netherlands: Schouten J. Bergen; Norway: Gulsvik A; Omenaas E; Svanes C and Laerum B. Barcelona; Spain: Anto´ JM; Sunyer J; Kogevinas M; Zock JP; Basagana X; Jaen A and Burgos F. Huelva; Spain: Maldonado J; Pereira A and Sanchez JL. Albacete; Spain: Martinez-Moratalla Rovira J and Almar E. Galdakao; Spain: N. Muniozguren and I. Urritia. Oviedo; Spain: F. Payo. Uppsala; Sweden: C. Janson; G. Boman; D. Norback and M. Gunnbjornsdottir. Gothenburg; Sweden: K. Toren; L. Lillienberg; A. Dahlman-Hoglund and R. Sundberg. Umea; Sweden: E. Norrman; M. Soderberg; K.A. Franklin; B. Lundback; B. Forsberg and L. Nystrom. Basel; Switzerland: N. Kunzli; B. Dibbert; M. Hazenkamp; M. Brutsche and U. Ackermann-Liebrich. London; UK: P. Burney; S. Chinn and D. Jarvis. Norwich; UK: D. Jarvis and B. Harrison. Ipswich; UK: D. Jarvis; R. Hall and D. Seaton. Portland; OR; USA: M. Osborne; S. Buist; W. Vollmer and L. Johnson.
File in questo prodotto:
Non ci sono file associati a questo prodotto.

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2318/122438
Citazioni
  • ???jsp.display-item.citation.pmc??? 21
  • Scopus 44
  • ???jsp.display-item.citation.isi??? 37
social impact