Lack of association between atopic asthma and the tumor necrosis factor alpha-308 gene polymorphism in a Czech population
Language English Country Spain Media print
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
12530118
Knihovny.cz E-resources
- MeSH
- Alleles MeSH
- Asthma genetics MeSH
- Hypersensitivity, Immediate genetics MeSH
- Adult MeSH
- Gene Frequency MeSH
- Genotype MeSH
- Introns MeSH
- Humans MeSH
- Lymphotoxin-alpha genetics MeSH
- Polymorphism, Genetic genetics MeSH
- Promoter Regions, Genetic MeSH
- Case-Control Studies MeSH
- Tumor Necrosis Factor-alpha genetics MeSH
- Check Tag
- Adult MeSH
- Humans MeSH
- Male MeSH
- Female MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Geographicals
- Czech Republic MeSH
- Names of Substances
- Lymphotoxin-alpha MeSH
- Tumor Necrosis Factor-alpha MeSH
Susceptibility to the development of asthma and other atopic diseases is known to be associated with genetic components. Several investigators have linked the tumor necrosis factor (TNF) genes and nearby markers located on chromosome 6p to atopy and asthma. A recent study has demonstrated that the TNF-alpha*2 allele of a polymorphism in the TNF-alpha gene promoter region (G-308 A) is associated with a higher risk for the development of atopy in Spanish patients. This study evaluates the possible role of two described bi-allelic polymorphisms in the TNF locus [a G to A transition at position-308 in the 5'-promoter region of the TNF-alpha gene and an NcoI restriction fragment length polymorphism (RFLP) in the first intron (+252A/G) of the LT-alpha(TNF-beta) gene] in atopic diseases in a Czech population. We investigated the distribution of these polymorphisms in a case-control study. The genotypes were determined in 151 patients with atopic asthma and 155 randomly sampled control subjects. The genotype frequencies for both polymorphisms were similar in cases and controls. No significant differences in allele frequencies were found between either of the patients groups and the reference subjects. Similarly, there were no associations of any of the examined variants of the TNF genes with total IgE, specific IgE or pulmonary function tests in patients with allergic diseases. We conclude that these polymorphisms of the TNF genes are unlikely to contribute to atopic disease risk in our population. Significant associations that have been reported in other studies may reflect the genetic heterogeneity of these complex diseases.
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