PMID- 16759385
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20070702
LR  - 20200928
IS  - 1476-7961 (Electronic)
IS  - 1476-7961 (Linking)
VI  - 4
DP  - 2006 Jun 7
TI  - Cytokine gene polymorphisms and atopic disease in two European cohorts. 
      (ECRHS-Basel and SAPALDIA).
PG  - 9
AB  - BACKGROUND: Atopy and allergic phenotypes are biologically characterized by an 
      imbalanced T helper cell response skewed towards a type 2 (TH2) immune response 
      associated with elevated serum immunoglobulin E (IgE) levels. Polymorphisms in 
      cytokine genes might modulate regulation of the TH1/TH2 balance. We thus aimed at 
      reproducing our previous findings from a European study population on the 
      association of various cytokine polymorphisms with self-reported hay fever as 
      well as increased total and specific IgE levels in two comparable study 
      populations. METHODS: Two prospective Caucasian cohorts were used. In the Basel 
      center of the European Community Respiratory Health Survey (ECRHS, n = 418) ten 
      distinct cytokine polymorphisms of putative functional relevance were genotyped. 
      In the Swiss cohort Study on Air Pollution And Lung Disease In Adults (SAPALDIA, 
      n = 6003) two cytokine polymorphisms were genotyped. The associations of these 
      polymorphisms with atopy were estimated by covariance and logistic regression 
      analysis. RESULTS: We confirmed IL4, IL10, IL6 and IL18 as candidate genes for 
      atopic health outcomes. In the large, well-characterized SAPALDIA cohort the 
      IL6(-174G>C) and IL18(-137G>C) polymorphisms were associated with circulating 
      total IgE concentrations in subjects with hay fever. The IL18(-137G>C) 
      polymorphism was also associated with the prevalence of hay fever. CONCLUSION: 
      Comprehensive characterization of genetic variation in extended cytokine 
      candidate gene regions is now needed. Large study networks must follow to 
      investigate the association of risk patterns defined by genetic predisposing and 
      environmental risk factors with specific atopic phenotypes.
FAU - Imboden, M
AU  - Imboden M
AD  - Molecular Epidemiology/Cancer Registry, Institute of Social and Preventive 
      Medicine, University Hospital Zurich, Switzerland. imboden@medgen.unizh.ch
FAU - Nieters, A
AU  - Nieters A
FAU - Bircher, A J
AU  - Bircher AJ
FAU - Brutsche, M
AU  - Brutsche M
FAU - Becker, N
AU  - Becker N
FAU - Wjst, M
AU  - Wjst M
FAU - Ackermann-Liebrich, U
AU  - Ackermann-Liebrich U
FAU - Berger, W
AU  - Berger W
FAU - Probst-Hensch, N M
AU  - Probst-Hensch NM
CN  - SAPALDIA Team
LA  - eng
PT  - Journal Article
DEP - 20060607
PL  - England
TA  - Clin Mol Allergy
JT  - Clinical and molecular allergy : CMA
JID - 101152195
PMC - PMC1538621
EDAT- 2006/06/09 09:00
MHDA- 2006/06/09 09:01
PMCR- 2006/06/07
CRDT- 2006/06/09 09:00
PHST- 2006/02/07 00:00 [received]
PHST- 2006/06/07 00:00 [accepted]
PHST- 2006/06/09 09:00 [pubmed]
PHST- 2006/06/09 09:01 [medline]
PHST- 2006/06/09 09:00 [entrez]
PHST- 2006/06/07 00:00 [pmc-release]
AID - 1476-7961-4-9 [pii]
AID - 10.1186/1476-7961-4-9 [doi]
PST - epublish
SO  - Clin Mol Allergy. 2006 Jun 7;4:9. doi: 10.1186/1476-7961-4-9.